Essentials of Trauma Anesthesia and Intensive Care 9811156083, 9788184451931

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Essentials of Trauma Anesthesia and Intensive Care
 9811156083, 9788184451931

Table of contents :
Chp 1 Burden of Trauma
Chp 2 Trauma Care Systems
Chp 3 Triage and Trauma Scoring
Chp 4 Approach to a Trauma Patient and Anesthetic Considerations
Chp 5 Airway Management in Trauma
Chp 6 Perioperative Management of Laryngotracheobronchial Injuries
Chp 7 Maxillofacial Trauma
Chp 8 Pathophysiology and Management of Shock
Chp 9 Hemodynamic Monitoring in a Trauma Patient
Chp 10 Massive Blood Transfusion: MBT Protocols, Blood Components, Complications
Chp 11 Coagulopathy in Trauma: Pathophysiology and Management
Chp 12 Intravenous Anesthetic Agents
Chp 13 Acute Pain Management in Trauma
Chp 14 Regional Anesthesia Techniques in Trauma Patients
Chp 15 Traumatic Brain Injury
Chp 16 Thoracic Trauma and Anesthetist
Chp 17 Abdominal Trauma
Chp 18 Initial Approach to a Spine-Injured Patient and Anesthetic Considerations
Chp 19 Comprehensive Approach to a Patient with Musculoskeletal Trauma
Chp 20 Cardiac Trauma
Chp 21 Burns: Resuscitation and Anesthetic Management
Chp 22 Anesthetic Concerns in Pediatric Patients
Chp 23 Anesthetic Concerns in Geriatric Patient
Chp 24 Trauma in Pregnancy: Assessment and Anesthetic Management
Chp 25 Special Considerations in Ocular Trauma
Chp 26 Mechanical Ventilation in Trauma
Chp 27 Nutrition in the Critically Ill Trauma Patient
Chp 28 Infection Control in Trauma Intensive Care Unit and Operating Room
Chp 29 Fluid and Electrolyte Imbalance
Chp 30 Acute Kidney Injury in Trauma Patients
Chp 31 Critical Care Management of Traumatic Brain Injury
Chp 32 Intra-abdominal Hypertension and Abdominal Compartment Syndrome
Chp 33 Remote Location Anesthesia
Chp 34 Organ Donation After Brain Death
Chp 35 Role of Simulators in Trauma Skills and Management Training

Citation preview

Essentials of

Trauma Anesthesia and

Intensive Care

Dr Babita Gupta Additional Professor (JPNATC) Department of Anesthesiology, Pain Medicine and Critical Care All India Institute of Medical Sciences New Delhi


Essentials of Trauma Anesthesia and Intensive Care Published by Pawaninder P. Vij and Anupam Vij Peepee Publishers and Distributors (P) Ltd. Head Office: 160, Shakti Vihar, Pitam Pura Delhi-110 034 (India) Correspondence Address: 7/31, First Floor, Ansari Road, Daryaganj New Delhi-110002 (India) Ph: 65195868, 23246245, 9811156083 e-mail: [email protected] e-mail: [email protected]

© 2016 by Peepee Publishers and Distributors (P) Ltd.

All rights reserved No part of this publication may be reproduced or transmitted in any form or by any means, electronic, mechanical, photocopy, recording, translated, or any information storage and retrieval system, without permission in writing from the publisher. This book has been published in good faith that the material provided by authors is original. Every effort is made to ensure accuracy of material, but the authors, publisher and printer will not be held responsible for any inadvertent errors. In case of any dispute, all legal matters to be settled under Delhi jurisdiction only.

First Edition: 2016

ISBN: 978-81-8445-193-1

Late Shri B L Gupta I still hear your guiding voice like an angel Urging me to walk ahead during odd times, I can still feel your warm embrace Telling me to keep faith and walk the right path; You fill in strength in my failed steps even today, And take it to the path of successful satisfaction.

This book is dedicated to my beloved father, Late Shri B L Gupta, whose impressive career graph made way through many odd circumstances. His unquenchable thirst for knowledge battled all obstacles. His life has been an inspiration for all of us. We still derive strength from his hard work, honesty, dedication and disciplined lifestyle. This book is due to the incessant support and guidance of my husband, Anil Gupta, whose unlimited love has taken me through all impediments of life and inspired me to tirelessly work for this book. My little princess, Malvika, I can never thank her enough for her unconditional support and love. Without her understanding, this task would have been impossible to accomplish.

Foreword It is a pleasure to write a foreword for the book “Essentials of Trauma Anesthesia and Intensive Care” compiled and authored by Dr Babita Gupta and team. Trauma is a disease of modern society and attained epidemic proportion in the current millennium and consumes significantly to the financial burden (3% of GDP in India) on our health care system. It also poses with various challenges to all personnel caring for them. Trauma Anesthesia and Intensive Care has seen epochal changes in the last few years; thereby significantly improving the overall outcome of severely injured patients, who were once considered non-salvageable. The availability of state of art equipment and high standard of care provided at Jai Prakash Narayan Apex Trauma Center, All India Institute of Medical Sciences, New Delhi has paved the way to many such dedicated trauma centers across the country. Anesthesiologists are in a unique position to provide best care to a critically injured patient during his entire journey from emergency room to operating room to Intensive Care Unit and during follow-up. As a surgeon, I realize the tremendous importance of the role of anesthesiologist not only in airway management and resuscitation, but also in their ability to alleviate acute and chronic pain in an agonizing trauma patient, by multimodal approach. Trauma anesthesia and critical care is a growing specialty in India and other developing countries, and surprisingly, yet there is sparse published material in the form of book which can lucidly cover perioperative management of trauma patients. The book “Essentials of Trauma Anesthesia and Intensive Care” is one such effort to fill this void. Luminary and eminent faculty members in the field of Anesthesiology and Intensive Care have contributed to the book “Essentials of Trauma Anesthesia and Intensive Care”. The chapters of the book are simple to comprehend, focused, provide latest guidelines and moreover have been presented in an interesting way. The rich illustrations enhance the value of this book. I am sure this book will be of immense benefit to all the anesthesiologists and intensivists caring for trauma patients. I am also confident that it will find a place in the personal library of all anesthesiologists. I compliment and congratulate the whole team for tremendous endeavor, and wish them success!

Prof MC Misra Director, All India Institute of Medical Sciences and Chief, JPN Apex Trauma Center, AIIMS New Delhi


Preface The glory of medicine is that it constantly moves forward; there is always more to learn. The ills of today do not cloud the horizon of tomorrow, but act as a spur to greater effort—William James Mayo. In keeping with the lines of Mayo, we bring the readers a publication that is the first of its kind, offering a comprehensive overview of managing trauma patients through data and studies. This book is a humble effort to bring forth extensive insight and knowhow on managing trauma patients both perioperatively and in the intensive care unit. The burden of trauma is exponentially increasing around the world—even more so in India. Appropriate and timely management is critical to a positive outcome, warranting a sound approach and a solid understanding of the pathophysiology of trauma patients. The ATLS ® principles help protocolize the management of the emergency department; however, there is inadequate literature on trauma patient management in the operating room and thereafter in the intensive care unit. Anesthesiologists are often involved in the overall care of trauma patients in the emergency department, OR, and the ICU; therefore, they need continuing education to enhance their knowledge and skills. The contents of this book were chosen to address the lacunae in the knowledge and management of trauma patients and to keep physicians and anesthesiologists updated on the state of the art. Special emphasis have been given to topics such as airway management, head trauma, and thoracic and spine injury. One neglected, yet important, topic—brain death and subsequent organ donation—is discussed in detail. The inspiration for this book was the lack of a textbook that succinctly addresses this critical subject, especially in the Indian sub-continent. A bleeding polytrauma patient, in extremis, may initially appear to be a gruesome, non-salvageable case, prompting anesthesiologists to prematurely terminate resuscitative efforts. However, if appropriately managed during the initial phases, not only with correct scientific knowledge but also with empathy and compassion, a young, healthy, productive life can be saved, thus giving a feeling of gratification. No words can adequately express my gratitude toward Prof MC Misra, Director, All India Institute of Medical Sciences and Chief, JPN Apex Trauma Center. He has been a constant inspiration not only to me but to the entire medical fraternity as we work toward a common cause—providing high quality care to trauma patients. My sincere thanks go to Prof MK Arora for his invaluable support and guidance. It would have been difficult to write and finish this book without the moral support and positive attitude of my beloved teacher, Dr Bharati Tendolkar, who is a mother figure and constant inspiration for me. This book would not have been possible without the efforts, feedback, and suggestions of all co-authors, whose inputs provided a huge impetus for the project. The work of my dear colleagues and the staff at JPN Apex Trauma Center was always of the highest standards, whether it was providing photos, X-rays, or CT images. I owe gratitude to the technical staff of OT assistants and hospital attendants for their unconditional support. I am also obliged to Shri Narayanji, Anil Bhat and Lakhan for volunteering to complete photography and other jobs in the OR. My special thanks to Ms Pallavi Tiwari, who helped me throughout the editing process. I am sure this book will provide knowledge and translate into a better understanding of the effective management of trauma patients in the OR and the intensive care unit.

Enjoy reading! Babita Gupta

About The Book Dear Readers, It is my pleasure to introduce the book ‘Essentials of Trauma Anesthesia and Intensive Care’ and the chief author and editor, Dr Babita Gupta to the readers. This book extensively discusses the anesthetic and critical care management of various injuries and covers the recent guidelines in the management of a severely injured patient in the operating room and intensive care unit. All the chapters also concisely cover the initial management of various injuries. This book has been prepared by renowned faculty members in the field of Anesthesia and critical care. It is a comprehensive book written in a lucid style, and directed not only to all anesthesiologists and intensivists, but also emergency physicians, surgeons and orthopedic surgeons managing trauma patients. This book should prove to be useful to postgraduates, senior residents and consultants. The highlights of the book are: •

Burden of trauma

Role of anesthesiologist in acute trauma care

Initial approach to trauma patients

Anesthetic and critical care management in specific trauma, spine trauma situations such as, traumatic brain injury, thoracic trauma, cardiac trauma, spine trauma, musculoskeletal trauma and abdominal trauma

Principles of damage control surgery and damage control resuscitation

Massive transfusion protocols

Regional anesthesia with special emphasis on ultrasound-guided nerve blocks

Brain death and organ donation

No other textbook covers trauma management in such a comprehensive manner, the way ‘Essentials of Trauma Anesthesia and Intensive Care’ does. I am sure this book will definitely find its place in the top reference books in the armamentarium of all anesthesiologists and intensivists caring for trauma patients.

Dr Bharati Tendolkar Professor and Head Department of Anesthesiology and Critical Care LTTMC and Sion Hospital, Mumbai

Contributors Professor Department of Anesthesiology LTM Medical College and Sion Hospital Mumbai, India

Chandni Sinha MD Assistant Professor Department of Anesthesiology and Critical Care All India Institute of Medical Sciences Patna, India

Anjan Trikha MD

Chhavi Manchanda MD, FRCA

Professor Department of Anesthesiology Pain Medicine and Critical Care All India Institute of Medical Sciences New Delhi, India

St Elizabeth Medical Center of Boston Tufts University, Boston, USA Deven Juneja MD, FNB Sr Consultant and Coordinator Department of Critical Care and Emergency Medicine Sri Balaji Action Medical Institute New Delhi, India

Amala Kudalkar MD

Anju Gupta MD, DNB, MNAMS, PGCCHM Assistant Professor Department of Anesthesiology DSIC, New Delhi, India

Antara Gokhale MD, DNB, EDIC Consultant, Intensivist Royal Hospital, Muscat

Arunima Prasad MD Attending Consultant Department of Anesthesiology Fortis Hospital, Noida Ex-Resident (JPNATC) Department of Anesthesiology Pain Medicine and Critical Care All India Institute of Medical Sciences New Delhi, India

Hemangi S Karnik MD Professor Department of Anesthesiology LTM Medical College and Sion Hospital Mumbai, India

Kiran Kiro MD Assistant Professor Department of Anesthesiology and Critical Care GB Pant Hospital and Associated Maulana Azad Medical College New Delhi, India

Manish Kotwani MD Assistant Professor Department of Anesthesiology LTM Medical College and Sion Hospital Mumbai, India

Ashish Bindra MD, DM Assistant Professor (JPNATC) Department of Neuroanesthesiology and Critical Care All India Institute of Medical Sciences New Delhi, India

Ashok Kumar Saxena MD, DA, FAMS, FICA Professor Department of Anesthesiology and Critical Care University College of Medical Sciences and GTB Hospital New Delhi, India Babita Gupta MD Additional Professor (JPNATC) Department of Anesthesiology, Pain Medicine and Critical Care All India Institute of Medical Sciences New Delhi

Manpreet Kaur MD Assistant Professor Department of Anesthesia and Critical Care Lady Hardinge Medical College and Hospital New Delhi, India Minal Harde MD, DNB Associate Professor Department of Anesthesiology TN Medical College and BYL Nair Hospital Mumbai, India

Monica S Tandon MD Professor Department of Anesthesiology and Critical Care GB Pant Hospital and Associated Maulana Azad Medical College New Delhi, India


Essentials of Trauma Anesthesia and Intensive Care

Namita Baldwa MD, DNB Assistant Professor TN Medical College and BYL Nair Hospital Mumbai, India

Rakesh Garg MD, DNB, MNAMS, PDCCHM Assistant Professor (Dr BRAIRCH) Department of Anesthesiology and Critical Care All India Institute of Medical Sciences New Delhi, India

Naveen Malhotra MD, FICA Professor Department of Anesthesiology Pt BDS PGIMS, Rohtak Haryana, India

Navin Pajai MD Assistant Professor Department of Anesthesiology Seth GS Medical College and KEM Hospital Mumbai, India Neha Gupta MD Resident, Department of Anesthesiology and Critical Care University College of Medical Sciences and GTB Hospital New Delhi, India Nita D’Souza DNB Consultant, Ruby Hall Clinic Pune, India

Pradeep Bhatia MD Head, Department of Anesthesiology and Critical Care All India Institute of Medical Sciences Jodhpur, Rajasthan

Prashant Nasa MD, IDCCM, FNB, FCCP, FICCM, EDIC Specialist and Head, Critical Care Medicine NMC Speciality Hospital Al Nahda, Dubai (UAE) Praveen Talawar MD Assistant Professor Department of Anesthesiology Pain Medicine and Critical Care All India Institute of Medical Sciences New Delhi, India

Purva Mathur MD Additional Professor (JPNATC) Department of Microbiology All India Institute of Medical Sciences New Delhi, India

Rachna Wadhwa MD Professor Department of Anesthesiology and Critical Care University College of Medical Sciences and GTB Hospital New Delhi, India

Rashmi Ramachandran MD Additional Professor Department of Anesthesiology Pain Medicine and Critical Care All India Institute of Medical Sciences New Delhi, India

Senthil Packia Sabapathy K MD Resident Department of Anesthesiology Pain Medicine and Critical Care All India Institute of Medical Sciences New Delhi, India

Smita Prakash MD Senior Specialist VMMC and Safdarjang Hospital New Delhi, India

Sona Dave MD, DNB Professor Department of Anesthesiology TN Medical College and BYL Nair Hospital Mumbai, India Swati Chhabra MD Assistant Professor Department of Anesthesiology Pt BDS PGIMS, Rohtak Haryana, India

Sweta Salgaonkar MD Professor and Pain Consultant Department of Anesthesiology Seth GS Medical College and KEM Hospital Mumbai, India

Vimi Rewari MD, MAMS, FIMSA Professor Department of Anesthesiology Pain Medicine and Critical Care All India Institute of Medical Sciences New Delhi, India

Yash Javeri DA, IDCCM Director and Senior Consultant Apex Healthcare Consortium New Delhi, India

Contents SECTION I: INTRODUCTION TO TRAUMA AND TRAUMA CARE 1. Burden of Trauma Babita Gupta ................................................................................................................................. 1 2. Trauma Care Systems Babita Gupta ................................................................................................................................. 9 3. Triage and Trauma Scoring Chandni Sinha, Babita Gupta ..................................................................................................... 20 4. Approach to a Trauma Patient and Anesthetic Considerations Babita Gupta ............................................................................................................................... 32

SECTION II: AIRWAY CONSIDERATIONS 5. Airway Management in Trauma Babita Gupta ............................................................................................................................... 53 6. Perioperative Management of Laryngotracheobronchial Injuries Babita Gupta ............................................................................................................................... 82 7. Maxillofacial Trauma Babita Gupta ............................................................................................................................... 91

SECTION III: CIRCULATORY ISSUES 8. Pathophysiology and Management of Shock Amala Kudalkar, Babita Gupta ................................................................................................. 113 9. Hemodynamic Monitoring in a Trauma Patient Hemangi S Karnik, Manish Kotwani ......................................................................................... 132 10. Massive Blood Transfusion: MBT Protocols, Blood Components, Complications Smita Prakash ........................................................................................................................... 150 11. Coagulopathy in Trauma: Pathophysiology and Management Pradeep Bhatia ......................................................................................................................... 170

SECTION IV: ANESTHETIC DRUGS AND REGIONAL ANESTHETIC TECHNIQUES IN TRAUMA 12. Intravenous Anesthetic Agents Nita D’Souza, Babita Gupta ...................................................................................................... 187 13. Acute Pain Management in Trauma Sweta Salgaonkar, Navin Pajai ................................................................................................. 208 14. Regional Anesthesia Techniques in Trauma Patients Ashok Kumar Saxena, Neha Gupta, Babita Gupta, Rachna Wadhwa ................................... 228

SECTION V: SPECIFIC TRAUMA SITUATIONS AND ANESTHETIC MANAGEMENT 15. Traumatic Brain Injury Monica S Tandon, Kiran Kiro .................................................................................................... 254 16. Thoracic Trauma and Anesthetist Sona Dave, Minal Harde, Babita Gupta ................................................................................... 286

x Essentials of Trauma Anesthesia and Intensive Care

17. Abdominal Trauma Babita Gupta ............................................................................................................................. 323 18. Initial Approach to a Spine-Injured Patient and Anesthetic Considerations Babita Gupta, Praveen Talawar, Anjan Trikha ......................................................................... 342 19. Comprehensive Approach to a Patient with Musculoskeletal Trauma Babita Gupta ............................................................................................................................. 372 20. Cardiac Trauma Babita Gupta ............................................................................................................................. 404 21. Burns: Resuscitation and Anesthetic Management Naveen Malhotra, Swati Chhabra, Chhavi Manchanda ........................................................... 420 22. Anesthetic Concerns in Pediatric Patients Rakesh Garg, Anju Gupta ........................................................................................................ 430 23. Anesthetic Concerns in Geriatric Patient Rakesh Garg ............................................................................................................................ 445 24. Trauma in Pregnancy: Assessment and Anesthetic Management Babita Gupta, Rakesh Garg ..................................................................................................... 455 25. Special Considerations in Ocular Trauma Rakesh Garg ............................................................................................................................ 468

SECTION VI: CRITICAL CARE ISSUES 26. Mechanical Ventilation in Trauma Babita Gupta, Senthil Packia Sabapathy, Vimi Rewari ............................................................ 480 27. Nutrition in the Critically Ill Trauma Patient Antara Gokhale, Babita Gupta ................................................................................................. 494 28. Infection Control in Trauma Intensive Care Unit and Operating Room Purva Mathur ............................................................................................................................ 515 29. Fluid and Electrolyte Imbalance Prashant Nasa .......................................................................................................................... 545 30. Acute Kidney Injury in Trauma Patients Deven Juneja, Yash Javeri ........................................................................................................ 559 31. Critical Care Management of Traumatic Brain Injury Ashish Bindra ............................................................................................................................ 567 32. Intra-abdominal Hypertension and Abdominal Compartment Syndrome Babita Gupta, Manpreet Kaur .................................................................................................. 600

SECTION VII: MISCALLANEOUS 33. Remote Location Anesthesia Namita Baldwa, Sona Dave ....................................................................................................... 615 34. Organ Donation After Brain Death Babita Gupta, Arunima Prasad ................................................................................................. 626 35. Role of Simulators in Trauma Skills and Management Training Rashmi Ramachandran, Vimi Rewari, Anjan Trikha ................................................................ 658 INDEX .............................................................................................................................................. 667



Burden of Trauma Babita Gupta

KEY POINTS ♦ ♦ ♦ ♦ ♦ ♦ ♦ ♦ ♦ ♦

Trauma remains the leading cause of mortality, morbidity and hospitalization especially amongst young productive population globally. According to the World Health Organization (WHO), it has been estimated that 5.8 million deaths annually are attributable to injuries, which account for 12% of the world’s burden of disease and 9% of deaths worldwide. More than 9 deaths occur every minute from unintentional injuries and violence. Majority of the trauma victims are persons 1 through 44 years of age. Half of the injury-related deaths occur between the age of 15 and 44 years. Trauma remains a neglected disease in most of the developing countries including India. Road traffic accidents account for 25% of injury-related mortality, while suicide and interpersonal violence together contribute to another 25% of the total mortality worldwide. Approximately 400,517 deaths occurred in the year 2013 as compared to 259,625 in the year 2003, thus becoming a major concern for the society and the policy makers. Majority of the accidental deaths (377,758—94.3%) were due to un-natural causes, while natural calamities claimed the rest of accidental deaths (22,759—5.7%). Traffic accidents which include road accidents, rail-road accidents and other railway accidents are the major contributors of accidental deaths by un-natural causes. Road safety requires multi-pronged approach to decrease the number of accidents. The main components of prevention of accidents adopted by Government of India are: (1) Education, (2) Enforcement, (3) Engineering (road and vehicles), and (4) Emergency care.

INTRODUCTION An ‘injury’ or ‘trauma’ used interchangeably is defined as “a bodily lesion at the organ level, resulting from acute exposure to energy (mechanical, thermal, electrical, chemical or radiance) in amounts that exceed the threshold of physiological tolerance”.1 In some cases (e.g. drowning, strangulation), the injury results from an insufficiency of a vital element. 1 Trauma remains the leading cause of mortality, morbidity and hospitalization especially amongst young productive population. It has a huge socio-economic impact on the health care system, entire society, family and the individual. In last few decades, a better understanding of injuries and changing perception have demanded increasing attention of policy makers in the public health arena worldwide. There is increasing awareness and acceptance of injury as a public health problem and a

preventable disease, over the past decade. This has resulted in development and implementation of effective prevention programs; consequently, decreasing the death rate due to injuries in few nations. Although majority of the developed countries have improved their injury control efforts and developed organized trauma care systems, it still remains a neglected disease in most of the developing countries, including India. Based on the premise that understanding the severity of the disease is essential to prevent and treat it, this chapter attempts to provide a global and national overview of burden of injury. It is hoped that realization of the staggering numbers of injury-related deaths, disability and economic loss will raise an awareness of the importance of trauma as a public health issue and encourage one to take steps to curb this disease.

2 Essentials of Trauma Anesthesia and Intensive Care

GLOBAL BURDEN OF INJURY According to the World Health Organization (WHO) and Centers for Disease Control and Prevention (CDC), it has been estimated that 5.8 million deaths annually are attributable to injuries, which account for 12% of the world’s burden of disease and 9% of deaths worldwide.2,3 Injuries contribute to more loss of lives than cancer and heart disease together.4 More than 9 deaths occur every minute from unintentional injuries and violence. Burden of injury becomes even more significant as majority of the trauma victims are in persons 1 through 44 years of age.2 Half of the injuryrelated deaths occur between the age of 15 and 44 years. This is the most productive age group; not only for the family, but even for the society and nation. Injuries account for a significant contribution to the disease burden in all countries all over the world (Fig. 1.1).2 The highest numbers of injury-related deaths worldwide are in the South East

Asia and Western Pacific Regions (Fig. 1.2).2 The mortality in men as a result of injury is twice that as that of women in all parts of the world. Although death remains an important indicator of the severity of injury disease, it is essential to remember that with each death due to trauma there are many thousand injury victims, who survive with permanent disability. This loss of healthy and fit life can be quantified by the, ‘diseaseadjusted life years’ or ‘DALY’ which measures the total years of life lost from premature death as well as years of life lost from premature death and years of life lived with disability. One DALY is defined as one lost year of healthy life, either due to premature death or disability.2 The estimated total number of DALYs lost globally due to trauma is 182,555,000, with more than 50% of total DALYs lost being in South East Asia and Western Pacific Region (Fig. 1.3).2

The boundaries and names shown and the designations used on this map do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers of boundaries, Dotted lines on maps represent approximate border lines for which there may not yet be full aggrement. © WHO 2002. All rights reserved

Injury-related mortality rate (per 100 000 population) in WHO regions, 2000 Africa LMIC 118.8

Americas HIC 53.8

LMIC 76.2

Sout-East asia India 96.9

Other LMIC 75.0

Europe HIC 47.6

LMIC 131.5

Eastern Mediterranean HIC 51.1

LMIC 70.4

Western Pacific HIC 56.2

China 51.5

Other LMIC 78.4

HIC, High-income countries; LMC, Low- and middle-income countries. Fig. 1.1: Global injury-related mortality (Reproduced with permission from Injury Chart Book: A graphical overview of the global burden of injuries. Department of injuries and violence prevention. Noncommunicable diseases and mental health cluster. World Health Organization, Geneva, 2002)

Burden of Trauma

WPR 24%

AFR 15%

AMR 11%

EMR 7%


property damage, lost wages of the individual as well as the supporting family members, employer costs, insurance costs and other indirect losses are also taken into consideration. It would be impossible to calculate the actual loss, which can be caused by injury, as trauma not only causes economic loss, but also causes mental trauma, depression, stress and pain. It also does not consider the sexually transmitted diseases resulting from rape or the effects of malnutrition following war.2 CAUSES OF INJURY

EUR 16%

SEAR 27%

Fig. 1.2: Regional distribution of global injury-related mortality, 2000 – Total number of deaths = 5,062,0000. South-East Asia (SEAR) and the Western Pacific (WPR) constitute approximately 50% of the total number of injury-related deaths AFR: Africa; AMR: Americas; EUR: Europe; EMR: Eastern Mediterranean (Reproduced with permission from Injury Chart Book: A graphical overview of the global burden of injuries. Department of injuries and violence prevention. Noncommunicable diseases and mental health cluster. World Health Organization, Geneva, 2002)

WPR 23%

AFR 16%

AMR 10%

Injury can be categorized as intentional and unintentional injuries. The unintentional injuries are mainly road-traffic accidents (RTA), poisoning, falls, fires, drowning and other unintentional injuries, like exposure to cold, heat stroke, electric shock, etc. The intentional injuries include selfinflicted injuries (suicide), interpersonal violence (homicide), war and other intentional injuries. RTA accounts for 25% of injury-related mortality, while suicide and interpersonal violence together contribute to another 25% of the total mortality worldwide, thus reflecting the increasing stress levels and low tolerance of the society (Fig. 1.4).2 RTA attributes to around 1.26 million deaths and cause significant injuries in around 20–50 million population (Fig. 1.5). Approximately, 60% of the total number of DALYs lost worldwide due to RTA are among young adults aged between 15 and 44 years. More than 90% of the RTA occur in the developing world. Low- and middle-income countries, which account for 72% of the world’s population, have Other 17%

EMR 8%

Road traffic injuries 25%

War 6%

EUR 12%

SEAR 31%

Fig. 1.3: Regional distribution of global injury burden (DALYs lost), 2000 – Total number of DALYs lost = 182,555,000. SouthEast Asia (SEAR) and the Western Pacific (WPR) constitute approximately 50% of the total number of DALYs lost AFR: Africa; AMR: Americas; EUR: Europe; EMR: Eastern Mediterranean (Reproduced with permission from Injury Chart Book: A graphical overview of the global burden of injuries. Department of injuries and violence prevention. Noncommunicable diseases and mental health cluster. World Health Organization, Geneva, 2002)

Injury-related losses are estimated to be more than $500 billion annually worldwide, thus adding huge economic burden on the family, health care system and the government.2 The total cost would be even more staggering, if the

Poisoning 6%

Interpersonal violence 10%

Falls 6% Self-inflicted violence 16%

Fires 5% Drowning 9%

Fig. 1.4: Distribution of global injury mortality by cause, 2000 (Reproduced with permission from Injury Chart Book: A graphical overview of the global burden of injuries. Department of injuries and violence prevention. Noncommunicable diseases and mental health cluster. World Health Organization, Geneva, 2002)

4 Essentials of Trauma Anesthesia and Intensive Care

ESTIMATED GLOBAL BURDEN OF DISEASE BY 2020 Injury-related deaths are estimated to increase dramatically by 2020, with more than 1 in 10 people dying from injuries.2 It is expected that injury-related deaths, particularly RTA, interpersonal violence, war and self-inflicted injuries will increase significantly by 2020 globally. The major impact of the injury disease would be on low- and middle-income countries, as it is projected that RTA will increase by 80% in these countries. RTA and intentional injury will be among the leading causes of mortality. RTA, which ranked at 9th position in 1990 will be at 6th position in the year 2020, while the DALYs lost will gain 3rd position in 2020 as compared to 9th position in the year 1990.2 Considering road accidents as a “major health problem with a broad Fig. 1.5: Distribution of accidental deaths in various states, 2013 range of social and economic consequences which if not (From: Accidental Deaths and Suicides in India 2013, National addressed timely may affect the sustainable development of Crime Records Bureau, Ministry of Home Affairs) countries and hinder the progress towards Millennium 80% of RTA although they share only 52% of world’s development goals”, the United Nations has aptly proclaimed registered vehicles.2 This depicts disproportionally high 2011–2020 as the ‘decade of action of road safety’.5 The burden of RTA deaths relative to the level of motorization. global project will mainly work on the 5 pillars of ‘safe South-East Asia regions have highest proportion of RTA- system’ approach: 1. Road safety management; 2. Safe related mortality. It also accounts for more than 33% of the roads and mobility; 3. Safer vehicles; 4. Safe road users; 5 total number of DALYs lost worldwide due to road-traffic- and 5. Post-crash response. The implementation of global action plan could contain the increasing trend of RTA and related injuries. perhaps reverse it by the year 2020.5 Self-inflicted violence contributes to 16% of injuryrelated deaths, with highest suicide rates found in the Western BURDEN OF INJURY IN INDIA Pacific and European regions. Interpersonal violence attributes to 9% of total injury-related deaths, with 99% of India is a vast country with world’s one-fifth population homicidal deaths occurring in the low- and middle-income residing in it. It faces the challenge of dealing with triple countries.2 Young persons in the age group 15–44 years epidemics simultaneously, i.e. non-communicable diseases, communicable and infectious diseases and injuries. constitute 60% of the worldwide mortality due to interIncreasing urbanization at an exponential annual rate of 26% personal violence. and industrialization over last 2–3 decades has led to a steady Fall-related deaths account for 6% of total injury-related increase in the rate of unintentional injuries, crime and mortality, with 25% of all fatal falls occurring in high-income violence.6 countries.2 As compared to other causes of injury, fall-related In India, the data collection and compilation of accidental mortality is significantly higher in adults more than the age and suicidal deaths is mainly done by National Crime of 70 years, particularly females, than younger population. Records Bureau, Ministry of Home Affairs.7 The deaths are China has the highest fall-related injury, accounting for principally categorized as accidental, i.e. death caused by double the DALYs lost to this type of injury, as compared an accident (un-natural) or a natural calamity (natural), and to other regions in the world. suicides. Another source which provides information/data Fire-related burns and subsequent death attribute to 5% of total injury-related deaths worldwide; more than 95% of fatal fire-related burns occur in low- and middle-income countries. South-East Asian females have highest fire-related deaths, followed by African males.2 Children below the age of 5 years and elderly above 70 years have the highest firerelated mortality rates.

on various aspects of road traffic accidents and deaths is the Transport Research Wing (TRW) of the Ministry of Road Transport and Highways.8 This nodal agency presents report on ‘Road Accidents in India’ annually covering the various facets of road accidents in the country. According to the report published in 2013 by National Crime Records Bureau, the incidence of accidental

Burden of Trauma


(un-natural and natural) deaths has increased significantly during the period 2003–2013 with an increase of 54% in the year 2013, as compared to 2003.7 Approximately, 400,517 deaths occurred in the year 2013 as compared to 259,625 in the year 2003, thus becoming a major concern for the society and the policy makers. The rate of accidental deaths increased by 25.5% during the period 2003–2013; though the population growth was 15% during the same period.7 The suicidal deaths have also increased by 21.6% during the decade (2003–2013), with 134,799 persons committing suicide in the year 2013, as compared to 110,851 in 2003. On further evaluation of the accidental deaths in each state, Maharashtra had the highest number, which accounted for 15.7% of total deaths in the country. Madhya Pradesh, Tamil Nadu, Uttar Pradesh and Andhra Pradesh also had significant share in total injury-related deaths in the year 2013 (Fig. 1.5).7 Young population aged between 15 and 44 years accounted for 60% of total deaths in the country in the year 2013; 78% being males, while 22% were females. It is estimated that 3% of gross domestic product (GDP) (i.e. 100 billion USD) is lost to the Indian economy due to fatalities and accident injuries as compared to 2% in the developed countries.9 Around 3.5 million people in India are left with injury-related disability, among these 2 million are caused by RTA. In the year 2004, the DALYs lost due to RTA were 7.248 million in India.10

causes of deaths attributable to nature were heat stroke, exposure to cold, landslide, avalanche, earthquake, cyclone, flood and lightning.7 Although torrential rains, devastating floods, rampaging cyclones and tragic landslides hit the headlines year after year, but actually lightning and heatstroke claim maximum lives due to natural causes, followed by cold wave. When adjusted to population growth, mortality due to natural calamities has shown a declining trend over past 10 years, which in a way is reflection of improving capabilities of disaster mitigation measures and response.

Accidental Deaths

Increasing unemployment, poverty, and stress have all resulted in increasing number of suicidal deaths. Around 134,799 people committed suicide during the year 2013, accounting for 15 suicides every hour. Family problems and illness were the most common reasons for committing suicide, while other causes were bankruptcy, suspected illicit relation, poverty, dowry dispute, love affairs, failure in exams and drug abuse. Most of the males committed suicide due

Majority of the accidental deaths (377,758—94.3%) were due to un-natural causes, while natural calamities claimed the rest of accidental deaths (22,759—5.7%) in the year 2013 (Fig. 1.6). The un-natural causes of accidental deaths were mainly due to road accidents (34.3%), sudden deaths (7.8%), drowning (7.5%), railway and rail-road accidents (7.2%), poisoning (7.3%) and fire accidents (5.5%).7 The By electrocution 2.6

Traffic accidents which include road accidents, railroad accidents and other railway accidents are the major contributors of accidental deaths by un-natural causes. Road accidents claimed majority number of lives and contributed significantly to the total number of accidental deaths.8 Railroad and railway accidents, which are almost negligible in most of the developed countries, contribute significantly to the total number of deaths in India.7 Approximately, 7.2% of total accidental deaths occurred in the year 2013. A total of 1388 rail-road and 31,236 railway accidents occurred, which killed 1318 and 27,765 people, respectively, i.e. there is a 90% probability of death in rail-road or railway accident, according to the present data. A campaign educating people not to cross the railway track and heavy penalty on doing so is essential to reduce these accidents. Suicides

By road accident 34.3

By falls 3.2 By causes not known 5.0

By fire 5.5

By natural causes 5.7 By other un-natural causes 13.9 By rail-road and other railway accident 7.2

By poisoning 7.3 By drowning 7.5

By sudden deaths 7.8

Fig. 1.6: Distribution of accidental death in India by cause (natural and un-natural) in 2013 (From: Accidental Deaths and Suicides in India 2013, National Crime Records Bureau, Ministry of Home Affairs)

6 Essentials of Trauma Anesthesia and Intensive Care

to financial problems, while emotional and personal causes predominated in females. Self-employed persons and housewives contributed to more than 50% of suicidal deaths. The four states—Tamil Nadu, Kerala, Maharashtra and Andhra Pradesh accounted for 54.9% of suicide victims in the age group 60 years and above. The suicide rate (number of suicides per one lakh of population) in cities (13.3) was higher as compared to all-India suicide rate (11.0).7 Road Traffic Accidents RTA is the biggest killer, contributing to 36.4% of accidental deaths. Rapidly increasing number of vehicles with lack of proper road infrastructure, education, low compliance to follow traffic rules and lack of law enforcement are all responsible for increasing number of RTAs. Lack of service lanes, foot paths, cycle tracks, also increases the risk of road accidents. The total number of motor vehicles has increased exponentially at a compound annual growth rate of 10.5% during the period 2002–2012.8 Although the road networking has gained tremendous increase in recent years, it has not kept pace with the rapidly increasing number of vehicles.11 Moreover, the road design and the vehicle type do not meet international safety standards. According to the Road Transport and Highways research wing statistics, around 486,476 traffic accidents occurred in the year 2013, which resulted in the deaths of 137,572 injury victims, i.e. an average of one fatality per 3.5 road accidents.8 On translating these numbers into description of problem, it means one road accident occurs every minute and one road accident victim dies every 4 minutes. A large number of road accident victims are young people in the productive range. In the year 2013, the age profile of road accident victims revealed that persons aged 25 to 65 years had the greatest share of the 53.4% of total road accident fatalities, followed by the group aged 15–24 years, with a share of 32.5%. A severely injured patient (Injury Severity Score >16) is six times more likely to die in a developing country, such as India as compared to a developed country, reflecting lack of organized trauma care system in our country.12 Numerous small trauma centers are mushrooming over highways; however, they lack trained manpower and systematic approach to a trauma patient. Although India possesses only 1% of total motor vehicles in the world, it shares 6% of the global RTAs.13 The severity of road accidents measured as the number of persons killed in 100 accidents showed a slight increase in the year 2013 (28.3) from the year 2012 (28.2).8 Uttar Pradesh had the highest number of road accidental deaths, followed by Tamil Nadu and Andhra Pradesh. The total number of accidents occurring in the rural areas accounted for 54.2% (263,593) as compared to urban areas which

accounted for 45.8% (222,883) of total accidents.8 Rural areas had much higher death percentage (61.2% of total deaths) than urban areas (38.2%). This clearly reflects the poor health care and the need for improvising in-hospital trauma care and management in rural areas, more than the urban. India is a diverse nation with huge disparity in financial position, habits, culture and beliefs amongst people. Similar situation is observed on Indian roads, where vehicles belonging to the era of 3 different generations ply and share the road. There is a heterogeneous mixture of motorized and non-motorized vehicles on the road with various engine capacity, size and shape.14,15 As per a study conducted by transportation research and injury prevention program (TRIPP), it was observed that non-motorized vehicles share vary from 30–70% during peak hours in same cities.16 While high speed motorized vehicles are increasing rapidly, nonmotorized mode of transport, like bullock-cart, cyclerickshaw, bicycle, continue to share the scarce road space. Bicycle still remains a major mode of travel in low and middle class populace in rural areas, towns and even cities; albeit with no safety gadgets, like helmet or fluorescent lights in front and rear. Moreover no dedicated cycle lanes are present on roads, thus making them vulnerable to accidents. For planning preventive strategies and developing trauma care system, it is essential to know the type of vehicle mainly responsible and timing of accidents. Motorized vehicles were responsible for 94.5% of total road accidents in 2013. The highest number of road accident deaths was in people riding on two-wheeler, contributing 39,353 deaths (28.6%), while cars, jeeps, taxis, trucks, tempos and tractors also contributed significantly to road accidents (Fig. 1.7). The high rates of road accidents usually occur between 15:00 and 18:00 hours followed by 18:00 and 21:00 and 9:00 and 12:00 hours.8

Fig. 1.7: Distribution of road traffic accidents by the type of vehicle (From: Road Accidents in India 2013. Government of India: Ministry of Road Transport and Highways, Transport Research Wing)

Burden of Trauma

On analyzing the causal factors responsible for road accidents, driver’s fault was the single most important factor responsible for accidents, fatalities and injuries.8 Exceeding the permitted speed limit caused the highest number of accidents, followed by alcohol intake. Other common causes were non-use of helmets, non-obeyance of traffic rules and poor visibility. Overloaded vehicles and overcrowding are the common factors which increase the probability of accidents. Highways allow higher speed resulting in relatively higher number of accidents and severity. Around 28% of total road accidents occurred on highways in the year 2013, attributing to 33.2% in total number of persons killed in RTA.8 Road Safety Initiatives by Government of India A number of road safety initiatives were taken by the Government of India (GOI), State government and other non-government agencies in the recent past. A slight decline in the number of road accidents, number of persons injured and also the number of persons killed in road accident was observed. Decline in all three parameters was observed for the first time in two consecutive years, i.e. 2012 and 2013 (Table 1.1). Table 1.1: The total number of accidents, persons killed and persons injured in the year 2012 and 2013; a decline is seen in all three parameters in the year 2013 as compared to 2012 2012





Persons killed



Persons injured



(From: Road Accidents in India 2013. Government of India: Ministry of Road Transport and Highways, Transport Research Wing)

The National Road Safety Policy initiation taken by the GOI would probably improve the road safety and traffic management in the country and decrease the RTAs and subsequent death. This decade has been declared as the ‘decade of innovation for inclusive growth’ by the GOI, which would work on the resolution that ‘roads be built not only for the vehicles, but for the people, safety and services’. The GOI has recognized trauma as a major public health issue and laid down policies which include:8 (i)

Promoting awareness and road safety and the socioeconomic implications of RTA.

(ii) Establishing a road safety information database to enhance the quality of collection of data, transmission and analysis.


(iii) To review the standards of design of road from safety point of view and bring them up to international standards. (iv) Safer vehicles and safer drivers by strengthening the driver license and ensuring that safety features are present in the vehicles during designing and manufacturing. (v) Educating and training to create awareness amongst population by holding seminars and workshops. (vi) Enforcement of safety laws. (vii) Speedy and effective trauma care and management. (viii) Implementation of road safety. A dedicated national road safety board has been established which will oversee the matters related to road safety and establish effective strategies for implementing road safety policy. Road safety requires multi-pronged approach to decrease the number of accidents. The main components of prevention of road accidents adopted by Ministry of Road Transport and Highways are: (1) Education, (2) Enforcement, (3) Engineering (road and vehicles), and (4) Emergency care. The fifth ‘E’ element which is also looked at is ‘Enactment of appropriate legislative measures’. 8 The various components of the multi-pronged approach to enhance the road safety have been elaborated in Figure 1.8, with main focus on preventive measures, because “If trauma due to road accidents is a disease causing an epidemic, prevention is the only vaccine to control it”. Although GOI has taken a step forward towards injury prevention, a giant leap is required to organize trauma care system which mainly includes: Prehospital care facility, hospital networking and organization of in-hospital care which includes acute care and definitive management. At present, all the above mentioned elements are in rudimentary stage in the trauma care services in India, thus making the task of stakeholders and policy makers daunting and challenging. Sustained, aggressive efforts are required to curb the disease of trauma by effective preventive measures, strict enforcement of law and timely and appropriate treatment of trauma victim. SUMMARY Trauma claims a large number of human lives annually worldwide. The burden of trauma is evident by the monumental data of injuries and injury-related deaths. Although many developed countries have improved their injury control programs, and demonstrated a decrease in injury-related deaths, trauma remains a neglected disease in most of the developing countries, including India. Road traffic accident is the biggest killer. Although Government

8 Essentials of Trauma Anesthesia and Intensive Care ENFORCEMENT

EDUCATION • • • • •

Publicity campaigns on road safety awareness Refresher training for heavy vehicle drivers to improve their competency and capability Road safety education to school and college going students Setting up institution for driving training and research Use of media for increasing road safety awareness

• • • • • •

Tightening safety standards of vehicles Compulsory use of seat belts Mandatory use of helmet Strengthening the patrolling on national and state highways Enhancement of penalty on breaking traffic rules Banning use of alcohol/mobile phone while driving

Multi-pronged strategy to decrease road accidents ENGINEERING •

• • • •

Improving the safety of vehicles during manufacturing, operation and maintenance for both motorized and non-motorized vehicles Presence of air bags Provision of installation of at least one child restraint in motor vehicles Improving the design of road as per international standards Design and construction of road facilities taking into consideration the needs of non-motorized vehicles and pedestrians Use of retroreflective tapes to improve the visibility of bicycles at night


Identification of black spots and their treatment thereof Removal of liquor shops from national highways Radar control for speed limit and traffic lights Police around schools (safer way to school) Speedy and effective trauma care and management First aid at the sites of accident. Toll-free number for reporting of accidents Basic life-support and advanced life-support ambulances deployed on highways Hospitals alongside the national and state highways

Fig. 1.8 : Multi-pronged strategy adopted by Government of India to decrease road accidents

of India has taken few steps towards injury prevention, sustained, aggressive efforts are required to curb the disease of trauma by effective preventive measures, strict enforcement of law and timely and appropriate treatment of trauma victim. REFERENCES 1. Baker SP, O’Neill B, Karpf RS. The injury fact book. Lexington, MA, Lexington Books, 1984. 2. Injury Chart Book. A graphical overview of the global burden of injuries. Department of injuries and violence prevention. Noncommunicable diseases and mental health cluster. World Health Organization, Geneva, 2002. 3. Worldwide injuries and violence. Centers for disease control and prevention. Available from index.html (Accessed on 11th August 2015). 4. Oestern HJ. The health-political significance of trauma surgery in Germany and the social and economical consequences. In: Oestern HJ, Probst J, eds. Trauma Surgery in Germany [in German]. Berlin, Germany: Springer-Verlag 1997; 2:63–79. 5. UN Decade of Action. Available from http://www.fiafoundation. org/our-work/road-safety-fund/un-decade-of-action/ (Accessed on 12th August 2015). 6. Gupta A, Gupta E. Challenges in organizing trauma care systems in India. Indian J Community Med 2009;34:75–76. 7. Accidental deaths and Suicides in India 2013, National Crime


9. 10.



Records Bureau, Ministry of Home Affairs. Available from (Accessed on 12th August 2015). Road accidents in India 2013. Ministry of Road Transport and Highways. Available at: (Accessed on 12th August 2015). Gururaj G. Road traffic deaths, injuries and disabilities in India: Current scenario. Natl Med J India 2008;21:14–20. World Health Organization. Metrics: Disability-adjusted life year (DALY). Available at: burden_disease/metrics_daly/en/. Accessed on 12th August 2015. Ministry of Road Transport and Highways. Basic road statistics of India 2010-11, 2011-12, 2012-13. Available at: http://morth. on August 12, 2015. Mock CN, Jurkovich GJ, Nii-Amon-Kotei D, Arreola-Risa C, Maier RV. Trauma mortality patterns in three nations at different economic levels: Implications for global trauma system development. J Trauma 1998;44:804–14.

13. Joshipura MK, Shah HS, Patel PR, Divatia PA, Desai PM. Trauma care systems in India. Injury 2003;34:686–92. 14. Tiwari G. Traffic flow and safety: Need for new models in heterogeneous traffic. In: Mohan D, Tiwari G (eds). Injury Prevention and Control. London: Taylor and Francis 2000; 71–88. 15. Mohan D. Road safety in less motorised environments: Future concerns. Int J Epidemiol 2002;31:527–32. 16. Mohan D. The road ahead: Traffic injuries and fatalities in India. Delhi: Transportation Research and Injury Prevention Programme, Indian Institute of Technology; 2004.

Trauma Care Systems




Trauma Care Systems Babita Gupta


The increasing burden of trauma and recognition of trauma as a disease has prompted the development of organized trauma care systems in majority of developed nations. There is considerable evidence that there is decrease in mortality with the improved organization provided by a system for trauma management.

The main elements of trauma care system are prevention, notification, pre-hospital care, hospital reception and resuscitation, in-hospital acute and definitive care, and rehabilitation.

An effective trauma care systems must ensure seamless transition between each phase of trauma care to get the ‘right patient at right time to the right place’.

Trauma care systems in India are at an embryonic stage of development. Near total lack of trauma care system leads to delay in transportation of patient and inadequate in-hospital care, resulting in high mortality rate amongst severely injured patients.

Significant efforts are required not only by the individual state governments, but also by the central government, non-governmental organizations and private agencies to develop an organized trauma care system.

The various areas requiring active efforts are: awareness and education among public, developing a simple, sustainable, practical and efficient pre-hospital care system, improving in-hospital care, rehabilitation and quality control in trauma care during all phases of trauma management.

A lead role may be adopted either by Ministry of Health and Family Welfare or Ministry of Road Transport and Highways to govern the trauma care system.

Introduction of organized multidisciplinary trauma team can improve the patient outcome. The aim of establishing a trauma team is to perform several tasks during assessment and resuscitation of the patient with a ‘horizontal approach’. Anesthesiologists have a pivotal role in the trauma team.

INTRODUCTION Historically, there has been an inextricable connection between the existence of trauma care and conflict and war situations all over the world.1 Evidence of existence of trauma care comes from the ancient Roman and Indian history. In the 1st century AD, the Roman army had wellorganized trauma centers, called ‘valetudinaria’, which were staffed 24 hours by physicians.1 The history of trauma care in India dates back to 4th century BC. There is evidence that a system of trauma care may have existed in India, as documented in the Arthäshästra, an ancient treatise written by Chänäkya. The Indian army had an ambulance service, with well-equipped surgeons and women to bandage wounds as well as to prepare food. The surgeons, i.e. ‘shalyarara’,

were specialized in treating wounds, especially those inflicted by an arrow, as the bow and arrow was the traditional weapon used then.1 However, India could not keep pace with the modern trauma care systems which ensure seamless transition between each phase of trauma care starting from the time of injury to rehabilitation and eventually gets translated into decreased disability, mortality and the financial burden on a nation. TRIMODAL DEATH DISTRIBUTION Deaths due to trauma have a trimodal distribution pattern which implies that trauma-related mortality occurs in one of three peaks.2 The first peak is during early period, i.e. within seconds to minutes of trauma. The most frequent


Essentials of Trauma Anesthesia and Intensive Care

causes of death are apnea, rupture of heart or great vessels or traumatic brain injury (TBI). Prevention is the only way to decrease this peak. The second peak occurs due to mortality following extradural or subdural hematomas, liver or spleen lacerations, pelvic ring injuries and/or polytrauma causing severe hemorrhage. This peak occurs within minutes or hour following trauma. Majority of the deaths occur due to failure to maintain patent airway or significant blood loss, that are preventable causes with timely emergency care. The third peak of mortality occurs due to sepsis and multiorgan failure (MOF) and is observed days to weeks following injury. The 3rd peak is affected by the care provided during the preceding periods. Optimal care provided during the initial period of trauma management has shown to have long-term beneficial consequences.

with the improved organization provided by a system for trauma management.7,8

The concept of ‘Golden hour’ was first innovated by R Adams Cowley in 1972, which advocates treatment of a trauma patient to a designated trauma center within an hour of injury.3 This has shown to significantly improve survival rates in trauma patients. The principles of rapid transport and treatment during ‘golden hour’ are based on the data from French military during World War I. Patients treated within 60 minutes after injury had 10% mortality, whereas 75% mortality was seen in patients treated after 8 hours.4 The concept of Golden hour has been criticized due to limited scientific evidence;5 hence it would be appropriate to say that faster a trauma victim is evaluated for life-threatening conditions and resuscitated, better is the outcome. Evidence from developed countries indicates that 15–30% of road traffic accident deaths can be prevented when early rescue and retrieval and in-hospital treatment are provided in a wellcoordinated way.6

The main elements of trauma care system are prevention, notification, pre-hospital care, hospital reception and resuscitation, in-hospital acute and definitive care, and rehabilitation (Figs 2.1 and 2.2).9 The development of an effective trauma care system is a difficult process, which requires cohesive efforts from the political and medical facilitators. Almost all of the evidences of the effectiveness of improvements in the organization of trauma care services come from developed nations. No one trauma system is ‘the best’ and every country has to approach differently to the organization and implementation of trauma care system. An attempt has been made to provide an overview of trauma care system in few developed countries where the trauma care services are of high standard.

TRAUMA CARE SYSTEM The increasing burden of trauma and recognition of trauma as a disease has prompted the development of organized trauma care systems in majority of developed nations. There is considerable evidence that there is decrease in mortality

What is a Trauma System? A trauma system is a ‘preplanned, comprehensive, organized and coordinated effort in a defined geographic area that delivers the entire range of care to all injured patients and is integrated with the local public health system’.9 Trauma systems must make efficient use of the available health care resources and should be based on the requirements of the population served.10 It should provide effective care across the nation and should also have the ability to expand to meet the medical requirements of the community arising out of a man-made or natural disaster.10

Trauma Care System in Germany Trauma care system in Germany is one of the most wellorganized trauma care systems in the world with clear-cut guidelines and goals. It fulfils all the requirements to effectively tackle increasing number of trauma victims as well as mass casualties. The goals followed by the trauma care system in Germany are:11

Fig. 2.1: Main elements of an integrated trauma care system

Trauma Care Systems 11

Fig. 2.2: Trauma care system in most of the developed countries (Reproduced with permission from Cameron PA. Triaging the right patient to the right place in the shortest time. Br J Anaesth 2014;113:226–33)

ii. To ascertain effective pre-hospital treatment by qualified personnel as soon as possible

km.11 In each helicopter, there is a doctor and a paramedic with experience in managing a severely injured patient and expertise in performing life-saving procedures.

iii. To minimize transportation time

In-hospital Care and Rehabilitation

i. To decrease the treatment free interval

iv. Immediately transport trauma patients to appropriate level trauma center where highest standard of treatment is available Pre-Hospital Care A dedicated central telephone number for reporting trauma incident is available throughout the country. There are around 1000 emergency ambulances equipped with a paramedic and a doctor and 7500 rescue ambulances have 2 paramedics to manage less severely injured patients.12 The ground ambulances are complemented with helicopter emergency medical service (HEMS). The entire country is covered by a network of physician-staffed HEMS which is organized by the German automobile club (ADAC).12 There are around 52 helicopters which fly over 50,000 missions annually. The average flight time to the scene of accident is around 10–15 minutes.13,14 Each helicopter covers a radius of 50

Germany has around 110 level I trauma centers which provide initial care to around 50% of severely injured patients. Besides these level I trauma centers, there are 200 level II regional trauma centers, with facilities to manage moderate-severely injured patients. The basic care of a trauma patient can be provided at level III trauma center, which is linked to a network of 10–15 nearby hospitals. Furthermore, the admission and transfer of patients is regulated by the agreements between pre-hospital rescue systems and trauma centers in the trauma network. The early treatment provided to the trauma patient in hospital is based on the recommendations for diagnosis and treatment issued by the Guidelines Committee of the German Society of Trauma Surgery [Deutsche Gesellschaft für Unfallchirugie (DGU)] which are in accordance with the principles laid down by American College of Surgeons (ACS) in Advanced Trauma Life Support (ATLS®) course. The


Essentials of Trauma Anesthesia and Intensive Care

rehabilitation centers are owned by the insurance companies and the treatment is given in a centralized manner.11 In order to improve the quality of treatment of severely injured patients, multiple trauma working group of the DGU founded the German trauma registry in 1993. The data includes 4 different time points: admission, initial treatment, intensive care stay, discharge and 90-day mortality. Trauma Care System in Australia Australia is a vast and sparsely populated island continent with a mixture of the best possible with the best achievable trauma care systems. 15 The communication for an emergency situation can be made through mobile phone (cell phone or satellite), short wave radio or by conventional telephones. The emergency number used nationwide for ‘Emergency response systems’ is -0 0 0-, which in turn connects to the nearest appropriate emergency service facility through operators.15 There is also provision for personal ‘Emergency Position Indicating Radio Beacons’ (EPIRBS), which can be used in remote areas.16 It enables to locate a distress call by a central station through a satellite link. Six levels of trauma care, divided over two types of networks (metropolitan trauma network and rural trauma network) exist in Australia. In the urban areas, the trauma retrieval is mainly by ground ambulances, unless there are traffic problems or accident has occurred at distant location, where the air ambulances are preferred. All trauma patients with major injuries are transferred to tertiary referral hospitals, while minor injuries are taken to nearest medical facility. In the semiurban or rural areas too, road retrieval is the norm, unless the distance to be covered is more than 200 km. All the major injuries will eventually be directed to a tertiary care hospital, but en route first aid room and local hospital which has limited facilities without any surgical capabilities. The injured is then transported by road or air to a regional hospital, which has surgical facilities, but no cardiothoracic or neurosurgery facility. Patients requiring these services are transferred to metropolitan tertiary referral hospital. Many big companies situated at remote locations (especially mining) have developed and trained their own staff to provide first-aid and rescue in industrial accidents. Around 60 air ambulances cover approximately 80% of Australia and hence at times medical care may be delayed in remote areas.17,18 The only solution to provide initial care in remote areas is by telemedicine facility. All the ambulances are equipped with highly trained paramedic who can perform

life-saving interventions, such as rapid-sequence intubation in unresponsive patient, administer ketamine to alleviate traumatic pain and transfuse red cell concentrate in indicated patients. The RFDS, i.e. Royal Flying Doctor Service, founded by Reverend John Flynn provides an acute retrieval system in remote and inaccessible areas.18 These aircrafts are capable of flying in worst weather conditions and can reach any place within 2 hours. The aircraft retrieval system is partially financed by the federal and state governments and partly by private donations. In-hospital Care, Rehabilitation and Registry In Australia, all the citizens are ensured of access to the public medical system, which is provided by the state and federal governments. These services are financed both by the taxes as well as the ‘Medicare levy’.15 One can also opt for additional private health insurance funded by insurance companies. With this insurance, one can avail services in private hospitals also. Rehabilitation services are provided by 160 public hospital rehabilitation units apart from private hospital rehabilitation services. State-based and individual hospital-based trauma registries are maintained by National Trauma Registry Consortium, which was founded in 2005.15 Trauma Care System in United States (US) The importance of trauma care systems was first emphasized in US in the year 1970. Since then, the trauma systems in US have evolved into one of the most mature and advanced trauma care systems in the world. The trauma care facilities are classified into five different levels of care (level I–V) by the ACS.19 In the year 2010, there were 1600 trauma centers in 40 states.20 Level I trauma center provides highest level of care and function as tertiary referral facility, while levels IV/V can provide basic care and stabilization of the patient before transferring to a higher trauma center. The pre-hospital services are provided by ground ambulances as well as the HEMS.21 The emergency response number used nationwide is 9-1-1. Majority of the helicopters (71%) fly with one paramedic and one nurse and the physician accompanies in only 5% of HEMS trips. The trauma centers usually follow the guidelines developed by ACS Committee on Trauma in the ‘Resources for optimal care of the injured patient’.19 The in-hospital treatment is in accordance with the ATLS® protocols, which is usually led by a trauma surgeon. Care for a specific kind of injury or

Trauma Care Systems 13

subpopulation is provided in the rehabilitation centers. Currently, multidisciplinary rehabilitation centers offer rehabilitation services to polytrauma patients. The trauma registry is maintained by National Trauma Data Bank (NTDB®). It is one of the largest trauma registry data, containing around 860,964 in the year 2014.20 TRAUMA CARE SYSTEMS IN INDIA–CURRENT STATUS Trauma care systems in India are at an embryonic stage of development. Near total lack of trauma care system leads to delay in transportation of patient and inadequate in-hospital care, resulting in high mortality rate amongst severely injured patients. It has been estimated that the probability of dying is six times more in severely injured patient (ISS >16) in a country with no organized trauma system, such as India, as compared to a developed country with an established trauma system.22 Significant efforts are required not only by the individual state governments, but also by the central government, non-governmental organizations and private agencies to develop an organized trauma care system.

there is no law enforcement for minimum qualification of ambulance paramedic, essential equipment available in ambulance, specialist licensing of health personnel and quality control of the treatment a patient receives.24 Funding In India, only 0.5% of the population is covered by national insurance23 and almost all patients have to bear their own cost, unlike other developed nations, where almost all the citizens are covered by medical insurance. Government hospitals provide free treatment, but are often overburdened, and this may compromise the quality of treatment. India has made major progress in medical care, including trauma care, but they are mainly restricted to major cities and private corporate hospitals. Private hospitals offer treatment only on payment of fees, which may not be affordable to a poor trauma victim. It is noteworthy that all private hospitals are bound by law to provide emergency treatment to all trauma victims, irrespective of fee-payment. However, despite a Supreme Court ruling that prohibits hospitals from refusing severely injured patient, this is seldom practiced. Many times, these hospitals flout the norm and ask for a deposit before admitting critical patients.

Administrative Components Operational Components Lead Agency Notification Although the data of the total numbers of accidental deaths and suicides and road-traffic accidents are maintained by the National Crime Records Bureau (NCRB) and Ministry of Road Transport and Highways, there is no nodal government agency for planning, developing, implementing, integrating and monitoring trauma care system.23 Some sort of trauma care facility exists in few cities, but there is no uniformity in the trauma care nationwide due to void of leadership. Above all, the existing systems for trauma care, although elementary in nature, are restricted to urban areas. Trauma care systems are virtually non-existent in rural and remote areas. In a survey conducted by Academy of Traumatology, the overall responsibility for leading the system was not defined in 26% of the systems.23 Legislation There are no uniform laws to ensure early access to lifesaving treatment for trauma victims. Many private trauma centers are emerging at highways. These small hospitals also provide ambulances for patient transport. However,

Notification of trauma incident is the first and critical step in the trauma management. There is a lack of central or state government organized emergency ambulance services. Although police numbers are signposted along state highways, ambulance numbers are not. Accident victims are often taken to the nearest hospital either by relative or police or occasionally bystander. Centralized Accident and Trauma Services (CATS) in Delhi is an autonomous body of Government of Delhi providing free ambulance services to trauma victims since 1991.25 The central control room of CATS receives calls at ‘1099’ and ‘102’ (toll free numbers) on 12 telephone lines. CATS is also linked with police control room and fire service through wireless sets. An Emergency Management and Research Institute (EMRI), started in Andhra Pradesh to improve pre-hospital care is operating in the public private partnership mode.26 It can be accessed through telephone number 1-0-8. There are ongoing efforts at various places to build up pre-hospital transport system, but a uniform emergency access number needs to be established throughout the country.


Essentials of Trauma Anesthesia and Intensive Care

Pre-Hospital Trauma Care The six elements of the pre-hospital trauma care are: detection, reporting, response, on-scene care, in-transit care and transfer to definitive care.27 Pre-hospital trauma care with all the above elements is virtually non-existent and a major lacunae in the trauma care system of India, making the implementations of concept of ‘golden hour’ an unrealistic goal.28 In India, 30% of severely injured patients die before reaching the hospital.29 Medical care is not accessible within one hour in majority (82%) of accident victims.29 One of the published studies from Mumbai in 2004, showed that the average time between the accident and admission to hospital was 6 hours.30 Some attempts to improve pre-hospital care have begun in various parts of the country. However, most of the pre-hospital transport and care remain restricted to major cities and are not integrated with the hospitals. Transport of trauma victims in rural areas or small towns are often done by indigenous methods with the limited resources available to them.23 Majority of the ambulances are used as transport vehicles and treatment is seldom initiated in transit. The probable reason is lack of trained paramedic in the ambulance, as only 56% of the ambulances have one or more paramedics.12 The pre-hospital treatment provided by these personnel is inconsistent and unreliable and if any, is mainly limited to first-aid and basic care. Health care personnel providing definitive airway to maintain an unobstructed airway or relieving tension pneumothorax by needle decompression remains a far-reached goal. CATS was the first comprehensive initiative towards improvising pre-hospital care. In order to minimize the rescue time, 151 ambulances have been deployed all over Delhi at strategic locations.25 There are two paramedics in each ambulance. The central control room and the ambulance stations are also linked with wireless sets to facilitate two-way communication. CATS also organizes training courses for the paramedics. Emergency and Accident Relief Center (EARC), Ambulance Access for All (AAA) and EMRI are the other pre-hospital care service providers in Tamil Nadu, Maharashtra and Andhra Pradesh, respectively.31 Increasing number of vehicles on road, congested and narrow roads can cause difficulty in transporting a trauma patient in a four-wheeler or sixwheeler ambulance. In order to negotiate heavy traffic in urban areas and to provide care in the ‘golden hour’, Ambulance Mobike and Rescue Services (AMARS) was launched in November 2004 in Ludhiana by Christian

Medical College (CMC).32 AMARS was the first of its kind in the country. Similar bike ambulances were also started in Bengaluru. There are around 30 first responder bike ambulances stationed at strategic locations in and around Bengaluru (Fig. 2.3).

Fig. 2.3: First responder bike ambulance in Bengaluru

Most of the developed nations have rescue helicopters equipped with trained paramedics complementing the ground ambulances, incorporated in their trauma care systems. Air ambulances are operational in India for transporting critically ill patient from one hospital to another. However, rescue air ambulances for trauma victims do not exist in India till date. Moreover, the air ambulances operating in India are owned by private companies. The costs of their services are exorbitant, ranging from Rs. 100,000–150,000/hour, excluding the charges of the attending doctor and paramedical staff. None of the public hospitals have the air ambulance facility till date. Decisive Scheme and Inter-Hospital Transfer Majority of the trauma victims are taken to the nearest hospital, irrespective of the severity of injures and availability of resources in the hospital. Statutory provision to transfer the patient to appropriate trauma care facility by police/prehospital personnel beyond the jurisdictional boundaries are still lacking.23 Protocols and guidelines to triage the patients and shift them accordingly after communicating with the hospital in advance are yet to evolve.

Trauma Care Systems 15

There are no protocols or guidelines for inter-hospital transfers. Tertiary care facility is mostly restricted to major cities and transferring a patient from one hospital to another is often a difficult task. The burden of arranging for interhospital transfer from a small nursing home/hospital to specialized center is often borne by the relatives/attendants rather than being protocol-driven or by law enforcement. In-hospital Care Acute and definitive care of trauma patients are provided by government hospitals, private hospitals and huge number of small nursing homes/clinics across the country. There is no intimation of the arrival of a severely injured patient and hence no preparation can be made in advance. Set protocols for triaging patients exists in only 54% of the hospitals, which is problematic as it can delay timely care of a major trauma patient.23 The casualty medical officer is the only doctor available to provide initial resuscitation to a trauma victim in around 30% of the hospitals.23 The district and rural hospitals often lack adequate infrastructure, resources, basic equipment for resuscitation and trained manpower. Standard norms to govern the quality of care being delivered to trauma patients are missing in majority of hospitals. Organized state and national trauma registries or data collection systems are non-existent making objective evaluation of trauma care very difficult. The level I trauma centers are few in number and located mainly in big cities but with the active efforts of central government, the level I trauma centers will soon increase in numbers. A networking of trauma centers along the ‘Golden Quadrilateral’—i.e. north-south and west-east corridors of the highways have been planned by the Ministry of Health and Family Welfare (MOHFW). Under the plans of Pradhan Mantri Swasthya Suraksha Yojana (PMSSY) and MOHFW, 118 hospitals/medical colleges would be upgraded to develop trauma care facility. The proposed pan-India trauma care network envisages the availability of designated trauma care facility at every 100 km on the National highways. Jai Prakash Narayan Apex Trauma Center (JPNATC), All India Institute of Medical Sciences (AIIMS) is a level I trauma center in New Delhi, which is a major step taken by Government of India in providing an apex institute for high quality trauma care, education and research facility.33 Standardized and protocol-driven trauma care by dedicated trauma team and encouraging patient outcome results have stimulated the establishment of many other level I trauma centers across the country. The concept of ‘Golden hour’

and the importance of standardized and prioritized treatment have started disseminating by increasing popularity of ATLS® course of ACS in India. But, the goal of each trauma care provider following the ATLS® principles may take time. Education To ensure high quality uniform, competent, multidisciplinary care for every severely injured patient, all the members of trauma team including doctors, nurses and paramedics need to be trained. Trauma education is rapidly increasing and has gained momentum in India. The ATLS® program for doctors, conducted under the auspices of ACS, was started at JPNATC, New Delhi in the year 2009. At present, there are 8 approved and 17 proposed sites in India.34 With the pool of 4000 ATLS® providers and around 200 faculty, it is expected that the basic principles of trauma management will disseminate among others and spread widely in the country.34 Advanced Trauma Care for Nurses (ATCN) course is designed for the nurses, parallel to ATLS®. Apart from the training programs running under the auspices of ACS, Academy of Traumatology (India) provides trauma life support skills under the National Trauma Management Course (NTMC).23 This training program is mainly intended for doctors, and is being conducted at big centers. CATS also conducts training courses named ‘Basic course for Ambulance Personnel’ (BCAP) for the drivers and paramedics deployed in ambulances.25 Rehabilitation There are active efforts in improving pre-hospital care and acute care in the last decade, but the rehabilitation care in India still remains dismal. Care of a paraplegic, quadriplegic, amputee patient or a TBI patient with neurologic defect mainly remains the responsibility of family members. There are no rehabilitation centers which cater to trauma patients based on their needs. Overburdened government hospitals are unable to cater all the patients and private hospitals are unaffordable to a common man for a prolonged duration. Non-governmental and charitable organizations with social workers and volunteers can play a major role in the rehabilitation process. Research Significant experimental as well as clinical research work has been done in trauma care over the last 20 years in developed nations. The results of trauma research work


Essentials of Trauma Anesthesia and Intensive Care

can influence changes in the trauma system. The trauma research is not limited to acute trauma resuscitation and definitive care, but also includes accident research. The accident research unit evaluates the technical information, damage to the vehicles, injury mechanism and correlate with clinical data. This may subsequently help in developing more sophisticated injury-prevention strategies and vehicle-safety design. Trauma research in India is soon gaining momentum. But, a change in the academic environment is required. Instead of a single department or institution conducting research, it would be appreciated, if a scientific network is established and the data is pooled for research. A robust nodal agency is required to maintain trauma registry in urban, semi-urban and rural areas. This can help in studying the differences in injury-patterns in various demographic regions and delivery of trauma care in densely populated urban areas vis-à-vis rural trauma care and hence develop preventive strategies, study the lacunae and improve the trauma care. TRAUMA CARE IN INDIA—FUTURE PERSPECTIVE AND DIRECTIONS There has been an increase in awareness of trauma as a disease causing epidemic among the medical fraternity, government, non-government organizations as well as among public. The situation at present is disconcerting and challenging, but not as dismal as it was a decade ago. Concerted efforts are yet to be made by all stake-holders as well as the society to keep pace with the developed world in improving trauma care systems in India. There are few things which cannot be altered and there is no point worrying to change them.15 We cannot change the distances involved and the fact that majority of population still reside in rural India, and in order to save a severely injured patient in remote location, we need to be dependent on basic first aid skills and on-site resuscitation. We need to develop indigenous trauma care systems depending on the prevailing local circumstances at low costs. The various areas requiring active efforts are:

• • • • •

Awareness and education among public Advanced pre-hospital trauma care system In-hospital care Inter-hospital transfer Trauma registry and research

Awareness and Education Among Public The first responder to an accident is usually the bystander or relative. The role of bystander is critical; even the most advanced and well-equipped trauma care system is futile, if the seriousness of the situation is not recognized by the bystander and fails to call for help.35 The first tier of a system can be established by educating public to recognize an emergency situation, call for help and provide basic care until formally trained healthcare personnel arrive. The five basic actions can be performed by bystanders at the site of accident, as designed in the American program.35 They are: 1. Stop to help 2. Call to help 3. Assess the victim 4. Start the breathing 5. Stop the bleeding People who have acquired this training are encouraged to keep basic items for resuscitation, such as gloves and bandages, so that they can provide first-aid. It is observed that the bystanders usually hesitate to help an injured victim and transport him to hospital. The reluctance is stemmed from the fear of getting dragged into protracted police investigations and legal proceedings. A new set of ‘Good Samaritan Guidelines’ were issued by the Ministry of Road Transport and Highways in May 2015. These guidelines were issued in response to petition filed by SaveLIFE Foundation in the Supreme Court (Fig. 2.4). It will prevent the police or a hospital from detaining a bystander who brings an accident victim to a medical facility. They will protect the Good Samaritans from getting entangled in legal cases while helping strangers injured in accidents. These guidelines are a step forward and need to be publicized through social media to encourage early transport of trauma victims by the bystanders. The second tier of trauma care system can be provided at community level, by those who are trained in basic prehospital trauma care.35 These providers should have formal training in pre-hospital care and stabilization and transport of trauma victim to definitive medical facility without causing further harm. Most of the deaths in the first hour after trauma are due to airway compromise, respiratory failure or uncontrolled bleeding. All three can be treated with basic resuscitative measures and prevent a number of deaths from trauma. Other measures taken during this phase are proper wound care, immobilization of fracture, protection of spine,

Trauma Care Systems 17

MINISTRY OF ROAD TRANSPORT AND HIGHWAYS NOTIFICATION New Delhi, the 12th May, 2015 No. 25035/101/2014-RS.–Whereas the Hon’ble Supreme Court in the case of Savelife Foundation and another V/s. Union of India and another in Writ Petition (Civil) No. 235 of 2012 vide its order dated 29th October, 2014, inter alia, directed the Central Government to issue necessary directions with regard to the protection of Good Samaritans until appropriate legislation is made by the Union Legislature; And whereas, the Central Government considers it necessary to protect the Good Samaritans from harassment on the actions being taken by them to save the life of the road accident victims and, therefore, the Central Government hereby issues the following guidelines to be followed by hsopitals, police and all other authorities for the protection of Good Samaritans, namely:– 1. A bystander of Good Samaritan including an eyewitness of a road accident may take an injured person to the nearest hospital, and the bystander or Good Samaritan should be allowed to leave immediately except after furnishing address by the eyewitness only and no question shall be asked to such bystander of Good Samaritan. 2. The bystander or Good Samaritan shall be suitably rewarded or compensated to encourage other citizens to come forward to help the road accident victims by the authorities in the manner as may be specified by the State Governments. 3. The bystander or Good Samaritan shall not be liable for any civil and criminal liability. 4. A bystander or Good Samaritan, who makes a phone call to inform the police or emergency services for the person lying injured on the road, shall not be compelled to reveal his name and personal details on the phone or in person. Fig. 2.4: Good Samaritan guidelines issued by the Ministry of Road Transport and Highways

oxygen supplementation and circulatory support in a headinjured patient.36 Advanced Pre-Hospital Trauma Care System The third tier of care is advanced pre-hospital trauma care system. A simple, sustainable, practical and efficient prehospital care system is required for effective trauma care.35 The pre-hospital care should be integrated into the existing transportation infrastructure, health care and public health system in the country. The local factors and resources should be taken into consideration while organizing trauma care systems. The existing pre-hospital care system needs to be made robust by increasing the number of well-equipped ambulances, having uniform notification number nationwide and by educating paramedics deployed in the ambulance. All the ambulances being run by the government agencies or non-governmental organizations should have all the equipment for resuscitation available (Fig. 2.5) and should be routed through a common number i.e. either 1-0-2 or 1-0-8. Under the pan India trauma care network scheme, it has been envisaged that an ambulance will be available at every 50 km along the National Highways. Apart from

Fig. 2.5: An advanced life support ambulance, with all the equipment and monitoring devices available to transport a trauma patient and treat in transit


Essentials of Trauma Anesthesia and Intensive Care

training paramedics in basic life skills, a protocolized decisive scheme for shifting a trauma patient based on his injuries considering the distance to be travelled is required. In-hospital Care A further essential step is improving in-hospital trauma care (acute care and definitive care). The level I trauma centers have been established in major cities. Small cities, towns and rural areas lack trauma care facility. However, establishing innumerable dedicated level II and level III trauma centers should not be the goal as it may involve huge financial burden on state governments and/or central government.33 Instead, the existing medical facility should be upgraded to provide treatment to a severely injured patient.33 Skill-based training programs for doctors and nurses are required. It should be emphasized that even if facility is not capable of providing definitive treatment to an injured patient, they should be able to recognize and address life-threatening situations and transfer the patient to an appropriate medical facility after proper communication. Legislative and statutory endorsement for inter-hospital transfer of patients beyond geographical boundaries is an important element of trauma care system. Inter-hospital agreements should be in place since many times a severely injured patient may be transported to a hospital with an inappropriate level of care and subsequently require secondary transport to another hospital with higher level of care within the trauma care system. Assessment, reviews and improvement is a continuous process and is essential to create and sustain a high quality trauma care program. The trauma care services should be strengthened by continuous quality control, which can be achieved by institution of trauma registry with validated indicators to track performance. This will enable us to understand the trends and assess the impact of interventions on patient outcome. A lead role may be adopted either by Ministry of Health and Family Welfare or Ministry of Road Transport and Highways to integrate all phases of trauma care and govern the trauma care system. Regardless of which lead agency holds the primary responsibility, all appropriate government sectors (e.g. transport, health, finance, urban and rural development) must be involved in planning and commissioning the system. TRAUMA TEAM Presence of various specialties in a trauma center can decrease mortality was first concluded by Adams Cowley.37 Improvement in the patient outcome has been observed with

the introduction of organized multidisciplinary trauma team.38,39 The aim of establishing a trauma team is to perform several tasks during assessment and resuscitation of the patient with a ‘horizontal approach’. This can decrease the time from injury to critical interventions, which can eventually have a direct impact on the patient outcome.40 The trauma team comprising anesthesiologist, surgeon, orthopedic surgeon, neurosurgeon and radiologist have to work in close coordination to achieve the goal of rapid and appropriate assessment and management. The trauma team composition varies from hospital to hospital in India; however, a surgeon, anesthesiologist and/or emergency physician are critical. The trauma team also includes nurses, technicians and health care provider. The team can be led either by a surgeon or an anesthesiologist or an emergency medicine physician depending on the hospital policy. The role of team leader is to ensure adherence to ATLS® guidelines by all team members, coordinate the resuscitation, decide which additional tests should be done and formulate a definitive plan.40 Anesthesiologists have a pivotal role in the advancement of major trauma care. They are skilled to manage difficult airway, treat shock, perform invasive procedures expeditiously and are also key providers of care in TBI. In European practice, it is not unusual to find an anesthesiologist working in pre-hospital environment, or in the emergency department (ED) as ED director or as a hospital trauma team leader.41 However, very few anesthesiologists in India work exclusively in the trauma center or are the trauma team leaders in the ED. This may be due to anesthesiologists’ reluctance to work outside operating room, shortage of anesthesiologists or the administrative decision. This is rather unfortunate since trauma is a rapidly evolving field of study presenting with unique challenges and appropriate care during initial period can improve the patient outcome.41 In case anesthesiologist is not a part of the team involved in trauma reception and resuscitation, there must be set protocols and procedure for an anesthetic call out in the ED. These protocols must mainly include difficult airway management, difficult ventilation and providing analgesia and/or anesthesia for pain relief or performing invasive procedures in the ED. SUMMARY Ubiquitous access to trauma care facility, prompt delivery of infield and in-hospital care for every citizen requires systemization of trauma care systems. Trauma care systems must emphasize on injury-prevention and rehabilitation along with implementation of pre-hospital care and advanced in-

Trauma Care Systems 19

hospital care. It should be able to address the daily demands of trauma care and form the basis of disaster preparedness. REFERENCES 1. Trunkey DD. The emerging crisis in trauma care: A history and definition of the problem. Clinical Neurosurgery 2007;54: 200–05. 2. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support Manual, 9th ed., Chicago, 2012. 3. Tobin JM, Vaaron AJ. Update in trauma anesthesiology: Perioperative resuscitation management. Anesth Analg 2012; 115:1326–33. 4. Santy P. Shock tramatique dans les blessures de guerre, analysis d’observations. Bull Med Soc Chir 1918;44:205. 5. Lerner EB, Moscati RM. The golden hour: Scientific fact or medical “urban legend”? Acad Emerg Med 2001;8:758–60. 6. McDermott FT, Cordner SM, Tremayne AB. Reproducibility of preventable death judgments and problem identification in 60 consecutive road trauma fatalities in Victoria, Australia. Consultative committee on road traffic fatalities in Victoria. J Trauma 1997;43:831–39. 7. Cameron PA, Gabbe BJ, Cooper DJ, Walker T, Judson R, McNeil J. A statewide system of trauma care in Victoria: Effect on patient survival. Med J Aust 2008;189:546–50. 8. MacKenzie EJ, Rivara FP, Jurkovich GJ, et al. A national evaluation of the effect of trauma-center care on mortality. N Engl J Med 2006; 354: 366–78. 9. Trauma System: Agenda for the future. Coordinated through the American Trauma Society Supported by the US Department of Transportation, National Highway Traffic Safety Administration. March 2004. Available from traumasysweb_04-21-10.pdf. (Accessed on 29-09-2015). 10. Guidelines for essential trauma care. World Health Organization 2004. Available from: prevention/publications/services/guidelines_traumacare/en/ (Accessed on 29-09-2015). 11. Westhoff J, Hildebrand F, Grotz M, et al. Trauma care in Germany. Injury 2003;34:674–83. 12. Hans-Joerg Oestern, Garg B, Kotwal P. Trauma care in India and Germany. Clin Orthop Relat Res 2013;471:2869–77. 13. Lefering R. AG Polytrauma der DGU. Jahresbericht fu¨r das Jahr 2010. Cologne, Germany: Lehrstuhl fu¨rUnfallchirurgie/ Orthopa¨die der Universita¨t Witten-Herdecke, Klinikum Ko¨lnMerheim; 2011. 14. Deutsche Gesellschaft fu¨r Unfallchirurgie [German Society of Trauma Surgery]. Weißbuch Schwerverletztenversorgung [Whitebook on the Care of the Severely Injured], 2006. Updated 2012. Available at: schwerverletzte/ weissbuch-schwerverletztenversorgung.html. Accessed on 29-09-2015. 15. Croser JL. Trauma care systems in Australia. Injury 2003:34: 649–51. 16. Search and rescue in the snowy mountains. Available from: Jindabyne, Perisher Valley, Khancoban and Tumut. Accessed on 29-09-2015. 17. Staemmler M, Walz M, Weisser G, Engelmann U, Weininger R, Ernstberger A, et al. Establishing end-to-end security in a nationwide network for telecooperation. Stud Health Technol Inform 2012:180:512–16.

18. Royal Flying Doctor Service. Available from: http://www. (Accessed on 29-05-2015). 19. American College of Surgeons. Resources for optimal care of the injured patient. Am Coll Surg 2014. 20. Hofman, Pape HC. Trauma care systems. In: Hans-Jong Oestern (eds). General Trauma Care and Related Aspects: Trauma Surgery II,1st ed. Heidelberg: Springer Science 2014; 1–18. 21. Blackwell T, Kellam JF, Thomason M. Trauma care systems in the United States 2003;34:735–39. 22. Mock CN, Adzotor KE, Conklin E, Denno DM, Jurkovich GJ. Trauma outcomes in the rural developing world: Comparison with an urban level 1 trauma center. J Trauma 1993;35:518–23. 23. Joshipura MK, Shah HS, Patel PR, Divatia PA, Desai PM. Trauma care systems in India. Injury 2003;34:686–92. 24. Sethi AK, Tyagi A. Trauma untamed as yet. Trauma Care 2001;11:89–90. 25. Centralised accident and trauma services. Available from: http:// b98ffd9f4944 2c8380/CATS1.pdf. (Accessed on 29-09-2015). 26. Emergency management and Research Institute (EMRI). Available from: (Accessed on 29-09-2015). 27. McLellan BA. Trauma severity scoring: The language of trauma. In: McMurty RY, McLellan BA, editors. Management of Blunt Trauma. Williams and Wilkins: Baltimore 1990;11–19. 28. Joshipura MK. Trauma care in India: current scenario. World J Surg 2008;32:1613–17. 29. Deshmukh VU, Ketkar MN, Bharucha EK. Analysis of trauma outcome using the TRISS method at a tertiary care centre in Pune. Indian J Surg 2012;74:440–44. 30. Murlidhar V, Roy N. Measuring trauma outcomes in India: An analysis based on TRISS methodology in a Mumbai university hospital. Injury 2004;35:386–90. 31. Anand L. Prehospital trauma care services in developing countries. Anaesth, Pain & Intensive Care 2013;17:65–70. 32. AMARS. Available from (Accessed on 29-09-2015). 33. Gupta A, Gupta E. Challenges in organizing trauma care systems in India. Indian J Community Med 2009;34:75–76. 34. Advanced Trauma Life Support 1International. Advanced Trauma Life Support1 (ATLS1) course of American College of Surgeons– India program. Available at: (Accessed on 29-09-2015). 35. Prehospital trauma care systems. World Health Organization 2005. Available from prevention/media/news/04_07_2005/en/ (Accessed on 29-092015). 36. World Health Organization.WHO road traffic injuries. Available at: (Accessed on 29-09-2015). 37. Cowley RA. Trauma center. A newconcept for the delivery of critical care. J Med Soc N J 1977;74:979–87. 38. Driscoll PA, Vincent CA. Organizing an efficient trauma team. Injury 1992;23:107–10. 39. Adedeji OA, Driscoll PA. The trauma team—A system of initial trauma care. Postgrad Med J 1996;72:587–93. 40. Groenestege-Kreb DT, O. van Maarseveen, Leenen L. Trauma Team. Br J Anaesth 2014;113:258–65. 41. Maureen McCunn, Grisson TE, Dutton RP. Anesthesia for trauma. In:Miller RD (ed). Miller’s Anesthesia, 8th edition. Philadelphia: Elsevier Saunders 2015;2423–59.


Essentials of Trauma Anesthesia and Intensive Care



Triage and Trauma Scoring Chandni Sinha, Babita Gupta


Majority of the deaths due to trauma are because of delay in presentation to the hospital and timely interventions. Optimization of both, prehospital and initial hospital care by proper triage is important.

Triage refers to the process of prioritizing the patients’ treatment based on the availability of medical resources.

Various triage scores have been formulated, which act as tools for trauma personnel to facilitate proper triage and to measure the outcome in trauma patients.

The trauma scores can be categorized into three main groups, depending on the criteria considered to calculate: 1. Physiological criteria, 2. Anatomical criteria, and 3. Combined anatomical and physiological criteria.

Ideal trauma methodology should also take into account the age, pre-injury health status and prehospital physiological data of the patients. Though there are many trauma scores in number; they are not free of limitations. Further research will refine the present scoring systems and improve their accuracy.

INTRODUCTION Trauma is the leading cause of mortality in patients under the age of 35 years.1 It has been estimated that by 2020 it will become the third leading cause of morbidity and mortality in all age groups.2 Death due to trauma has a classical trimodal distribution.3 The first peak occurs within minutes of the assault, wherein there is injury to the brain, heart and spinal cord. The second peak is within hours, where death usually results from major blood loss, e.g. liver injury, splenic injury, etc. It is these patients whom we have to target, as timely intervention leads to prevention of many deaths. The third peak is due to deaths at a later stage due to complications, like sepsis and multiple organ dysfunction syndrome (MODS). The importance of platinum 10 minutes for assessment and ‘golden hour’ for surgical intervention in trauma patients has been emphasized since long.4 These can be achieved by proper triage or selection of patients. Triage refers to the process of prioritizing the patients’ treatment based on the availability of the medical resources.5 The aim of triage is to be selective, so that the limited medical resources are available to the patients who will benefit the most.6 The word ‘triage’ originates from the French word

‘trier’ which means to sort.7 The term may have been originated from the work of surgeon in chief of Napoleon’s imperial guard, Dominique Jean Larrey. This word was reused during World War I by French doctors treating the wounded at the aid stations in the battlefield. The more seriously injured soldier would receive initial resuscitation followed by definitive care, while the soldiers with minor injuries would receive first-aid.These lessons were slowly translated into civilian practice. Earlier, the injured patients were taken to the nearest facility without any proper triage. Late 1970s saw the advent of Advanced Trauma Life Support (ATLS ® ) which emphasized the role of prehospital and in-hospital triage.8 PURPOSE The purpose of triage is to do the most good for most patients using the available resources. This is done by classifying the patients according to the severity of their injuries and prioritizing their transport, destination and treatment accordingly.5,9 Ideal triage systems would direct patients with more severe injuries to the appropriately staffed hospital while the not so severely injured patients to other hospitals. This will ensure better resource utilization and

Triage and Trauma Scoring 21

patient outcome.10,11 Shackford et al. showed that trauma centers improved the outcome of major trauma victims considerably, since they provided comprehensive multidisciplinary care to severely injured patients. 12,13 The process of triage was initially limited to prehospital settings, but its use has been extended to emergency department (ED) and the operating room (OR). GOALS OF TRIAGE 1. The primary goal of triage is to identify patients who need immediate care, without which they might suffer excessive morbidity and mortality.11 This requires rapid clinical evaluation, initial stabilization and transport of such patients to the appropriate medical facility. The concerned medical facility is informed before shifting the patient so as to prepare them with the personnel and equipment required. 2. The other goal is to identify critical patients who are unlikely to survive irrespective of the treatment they receive. This will help the triage personnel to divert the limited resources to other patients, who are likely to survive. 3. Improvement of the performance of the triage team is one of the important goals. This is done by evaluating one’s own performance at the end of mass casualty. Under-triage and over-triage scores have been used as markers of efficient triage system. Under-triage refers to underestimating the injuries of the patient. It is defined as the triage decision of classifying patients as not needing higher levels of care when in fact they do.14 It is a false negative triage decision. This results in patients not receiving adequate care which they are supposed to.15 An under-triage rate of 5–10% is considered acceptable.16 Over-triage refers to classifying patients as critical enough to require trauma center when in fact they do not. This results in the wastage of manpower, finances and resources.17,18 Despite this, over-triage rates upto 50% are acceptable. These rates are kept high with the aim of avoiding under-triage.19,20 TYPES OF TRIAGE 1. Simple triage: It is the first step at the site of accident wherein the patients who require immediate attention are sorted, stabilized and transported to the hospital. The triage personnel may label such patients with tags which display the patient findings and also help in identification of the patient.

2. Advanced triage: Doctors and trained nurses separate patients who will not survive irrespective of the treatment given to them. Such patients do not receive any treatment. This is done to divert the scarce resources to the patients who will benefit from them. 3. Reverse triage: There are few scenarios where sometimes the less wounded are treated in preference to the others. Such situations arise in the war, where an army might require its soldiers at the battle front. Conventional Triage Conventionally, in advanced triage, injured people are sorted into categories with corresponding colors and numbers (Fig. 3.1). 1. Black/expectant/deceased:21 These refer to patients who are so severely injured that they will die irrespective of the treatment they receive. Examples include large area burns, lethal radiation dose, cardiac arrest and severe head injuries. Their treatment is usually palliative. 2. Red/immediate: These patients are those who are severely injured but will respond to immediate treatment. Hence, they are first in the priority list and require immediate surgery or intervention. These include head injury, flail chest and internal injuries. 3. Yellow/observation: Their condition is stable for the moment, but will require observation and hospital care. These include compound fractures, amputation and maxillofacial injuries without airway compromise. 4. Green/wait/walking wounded: These patients do not require doctor’s care immediately. They may wait for few hours before being addressed to, e.g. simple fractures, soft tissue injuries. 5. White/dismiss/walking wounded: These patients have minor injuries. First-aid and home care are sufficient for them, e.g. minor cuts/abrasions. Retriage The physiological changes due to trauma is a dynamic process. A person might deteriorate or improve over time especially when the transport period is long. Retriage refers to the process of repeated assessment of the patients and sorting them accordingly. A worsening or improving clinical status might redirect resources towards or away from the patient. Rahmat et al. stated that though retriage increased


Essentials of Trauma Anesthesia and Intensive Care


Fig. 3.1: (a) Triage area at a Level I trauma center, with resuscitation bay/red area, (b) observation area/yellow area, (c) color coded triage bands, and (d) triage nurse tagging the patient with appropriate band

the workload of ED personnel, it reduced the waiting time of patients with worsening clinical condition.22 TRIAGE TOOLS Triage decision is the most difficult aspect of triage due to limitations of data and time. Triage officer must be able to rapidly assess the scene and also do a focused rapid assessment of the patients. Trauma scores have been formulated based on anatomical and physiological characteristics of the patients to characterize the nature and extent of injury. These scores act as a tool to measure the outcome in trauma patients and also help the triage personnel to take decisions. The outcome may refer to morbidity, length of ICU stay, mortality or other endpoints. These scoring systems form an essential component of effective trauma care, triage, clinical research and policy making.21,23

Till date, more than 50 trauma scores have been used, but none of them is devoid of limitations.24 Trauma scoring is depicted by a number indicating the severity of an injury. The trauma scores can be categorized into three main groups, depending on the criteria considered to calculate. 1. Physiological criteria a. Trauma Index b. Glasgow Coma Scale c. Trauma Score d. Revised Trauma Score e. CRAMS (circulation, respiration, abdominal injury, motor and speech response) Scale f. Emergency Trauma Score (EMTRAS)

Triage and Trauma Scoring 23

2. Anatomical criteria a. Abbreviated Injury Score b. Injury Severity Score c. New Injury Severity Score d. Anatomical profile 3. Combined anatomical and physiological criteria a. Trauma Revised Injury Severity Score b. International Classification of Disease Based Injury Severity Score Physiological Scores Physiological scores measure the acute dynamic component of an injury.25 This is of significance as most of the trauma deaths occur within hours due to disruption of normal physiology leading to respiratory failure, shock, brain and spinal cord injury.26-28 The various parameters used are heart rate, blood pressure, respiratory rate (RR), temperature etc. These parameters are easy to assess with simple physical examination. The data is ranked into numerical format and used in various scores. Greater deviation from normal reading represents more severe injury. Trauma Index The trauma index (TI) was one of the oldest trauma scoring methods developed to be used by non-physicians in the field.29,30 The variables included were: blood pressure, respiratory status, anatomical area, type of injury and central nervous system (CNS) status. Little correlation existed between TI and injury severity, thus limiting its widespread usage.31 Glasgow Coma Scale Glasgow Coma Scale (GCS) was first used by Teasdale and Jennet in 1974 to measure the functional status of the brain.32 Over time, GCS has become an integral part of various triage tools like, trauma score, revised trauma score (RTS), CRAMS scale and the trauma triage rule. GCS has been used to measure the functional status of the brain with eye opening, motor response and verbal response as its parameters. The best motor, verbal and eye responses are coded with values ranging from 1–6, 1–5 and 1–4, respectively. The GCS is scored from 3 to 15; with GCS >13 correlating with mild head injury, 9–12 with moderate head injury and GCS ≤8 with severe head injury. Studies

have concluded that best motor response is a strong predictor of outcome in head injured patients.33,34 Patients who follow simple commands have a better outcome than patients who do not. The validity of GCS has been tested over time in various studies.35-37 GCS correlates linearly with the morbidity and mortality in trauma patients.38,39 Limitations: 1. The assessment of GCS is difficult in sedated and paralyzed patient, which is a common treatment protocol practiced in head injured patients.40 The ‘motor only’ model is not reliable and cannot be used in patients who are paralyzed and in patients with high cervical spine injuries with neurologic deficits. 2. The function of the brain can be affected by various other factors and affect the GCS, e.g. electrolyte derangement, hypoglycemia, severe sepsis, etc. 3. Some authors are of opinion that ‘Best eye opening response’ subscore is not required as it is sometimes not possible to elicit the response; and adds little to the predictive value.41 Trauma Score The 1980s saw the advent of Trauma Score (TS) which was a modification of a previously used triage index. Trauma score ranged from 1 to 16 and included GCS, systolic blood pressure (SBP), capillary refill and RR.42 Score of 16 had the best prognosis while 1 was the worst. Patients with TS less than 12 were triaged to trauma center. Trauma score was a simple physiological measure, useful in both blunt and penetrating injuries.43 Limitations: 1. The drawback of this score was that it reported a low rate of inter-rater reliability as it included subjective criteria, like capillary refill and chest expansion.44 2. Furthermore, on retrospective analysis, TS was found to underestimate the condition of head injured patients. This led to the modification of trauma score, i.e. revised trauma score.27 Revised Trauma Score TS was modified to exclude capillary refill and chest expansion, both of which were difficult to assess in field condition. Two versions of the revised score have been developed, one for triage [Triage-RTS (T-RTS)] and another for use in outcome evaluations (coded RTS).45


Essentials of Trauma Anesthesia and Intensive Care

Triage-Revised Trauma Score: The sum of coded values of GCS, SBP, and RR is used in T-RTS. Each parameter ranges from 0–4, with the maximum score of RTS being 12 (Table 3.1). Patient with RTS less than 11 needs specialized trauma care and indicates transport to a designated trauma center. The cutoff value of 11 has increased the sensitivity; triaging nearly all the severely injured patients to the trauma center. T-RTS is a simple and sensitive tool with easily assessable parameters. Its usage has been validated in numerous studies.46,47 Coded RTS: The other form of the RTS is more complicated to calculate and its use is reserved for quality assurance and outcome prediction. The coded RTS is calculated as given below, wherein SBPc, RRc and GCSc represent the coded values of each variable: RTSc = 0.9368 GCSc + 0.7326 SBPc + 0.2908 RRc The advantage of coded RTS is that emphasis has been given to GCS, which has a significant impact on the outcome. Hence, RTS yields better outcome predictions in patients with severe head injury.

CRAMS (Circulation, Respiration, Abdominal Injury, Motor and Speech Response) Scale CRAMS scale is a simple and easy to evaluate trauma score developed for the field triage.48 The acronym represents circulation, respiration, abdominal injury, motor and speech response. These parameters are individually assessed and categorized according to abnormality (Normal: 2, mildly abnormal: 1, highly abnormal: 0). Score of more than 8 represents minor injuries and can be discharged. A score of 8 or less signifies major trauma indicating transfer of the patient to trauma center.49 The accuracy of CRAMS has been proven by prospective studies.50 However, Ornate et al. stated that CRAMS scale was not a sensitive tool as it failed to identify 2 out of 3 patients with major trauma.51 According to them, the clinical acumen of the paramedics handling such patients was better than this score. EMTRAS (Emergency Trauma Score)

1. The limitations are the same as for GCS, i.e. it is difficult to assess in sedated, intoxicated and paralyzed patients. Patients who are under the influence of drugs can be alternatively scored by using best motor and eye response and predicting the verbal response subscore. This has shown to have similar predictive value as calculating the whole GCS.

This physiological scale was developed by Raum et al. as an early predictor of mortality. The data was prospectively collected over a period of 10 years from the German Trauma Registry.52 The criteria taken into account are age, prehospital GCS, base excess (mmol/L) and prothrombin time. Each parameter is subdivided into four classes; scoring from 0 to 3. Scores of each class are summed to obtain the EMTRAS; ranging from 0 to 12. This is an easy to use scale with the parameters readily available in the ED. This scale was validated by Mangini et al. as an early predictor of mortality.53 More studies are required to prove the efficacy of this scale.

2. The complexity of coded R-TRS has limited its use in few countries, like North America.

Anatomical Indices


Table 3.1: Revised trauma score Coded value


SBP (mm Hg)

RR (breaths/min)









GCS: Glasgow coma scale; SBP: Systolic blood pressure; RR: Respiratory rate

Anatomical scores have been widely used to measure the severity of the injury. When used along with the physiological scores, their ability to measure the outcome increases. Abbreviated Injury Score (AIS) AIS is one of the most commonly used anatomical scales to assess injury. This system was first described in 1971 by the Association of Automotive Medicine for vehicular injuries.54 Since then it has been modified a number of times; the latest being in 2005 with an update in 2008. There are more than 2000 injuries listed in the latest update. AIS describes the type, location and severity of the injury (Table 3.2).

Triage and Trauma Scoring 25 Table 3.2: Abbreviated injury severity (AIS) injury ranking Numerical scale


Body region



Head and neck
















Limitations: 1. AIS measures a single injury. Hence, it does not predict patient outcome or mortality accurately.55 2. There is an internal inconsistency while using the severity scale. A score of 3 in one region might not correspond to 3 of another region. 3. There is no inclusion of scoring of open or compound femur fracture, which is an important factor for the functional outcome and morbidity. 4. The severity scale is ordinal in nature. The difference between AIS 1 and 2 is not the same as AIS 3 and 4.

Injury severity scale introduced by Baker et al. was the first scale to be used for measuring multiple injuries.56 ISS is an anatomical scoring system that provides an overall score for patients with multiple injuries. Each injury is allocated to one of six body regions (head, face, chest, abdomen, extremities including pelvis and external) and is assigned AIS. Only the highest AIS in each body region is used. The 3 most severely injured body regions have their scores squared and added together to produce the ISS. An example of the ISS calculation is shown in Table 3.3. The ISS takes values from 0 to 75. If Table 3.3: An example of injury severity scoring (ISS) calculation Region

Injury description


Square top three

Head and neck

Cerebral contusion




No injury



Flail chest



Minor contusion of liver Complex rupture spleen



Fractured femur



No injury


AIS: Abbreviated injury severity

Limitations: 1. The drawback of ISS is that it limits the contributing regions to only three and leaves the rest of the injured sites, which may contribute to morbidity and mortality. Also multiple injuries at the same site might not be accounted for. 2. ISS gives equal emphasis to all the six regions, with no increased importance to head injury. Hence, its ability to predict outcome in head injured patients is inconsistent. 3. Any error in calculating AIS increases the inaccuracy of ISS manifold. 4. It is not an effective tool in ballistic penetrating injury wherein there are multiple injuries in a single body area. 5. ISS does not take into account the physiologic variables.

Injury Severity Score (ISS)

Injury Severity Score: 50

an injury is assigned an AIS of 6 (unsurvivable injury), the ISS score is automatically calculated as 75. The ISS is virtually the only anatomical scoring system in use and correlates linearly with mortality, morbidity, hospital stay and other measures of severity.




Thus, ISS is not a reliable measure of injury severity and cannot be used to compare injuries of various population.57,58 Despite all these limitations, ISS continues to be widely used to characterize multiple injuries. New Injury Severity Score (NISS) A simple but significant modification of ISS is the new ISS or NISS, based on the 3 most severe injuries regardless of body region.59 One of the major drawbacks of ISS is that it fails to take into account multiple injuries in the same body region, irrespective of the severity of the injury. This often leads to underestimation of mortality especially in cases of head injury (with a combination of subdural, subarachnoid and extradural hemorrhage) and minor injuries in the rest of the body. NISS is a simple and user friendly anatomical measure of injury. It is a sensitive tool especially in head injury and penetrating injury. There are various studies suggesting NISS better than ISS as the standard measure of injury severity and as a predictor of survival.60-62 Limitations: Few studies suggest that NISS often leads to the overestimation of injury by giving undue importance to injuries in the same region and neglecting the rest.60,63


Essentials of Trauma Anesthesia and Intensive Care

Anatomical Profile (AP)




It is another anatomical scale introduced to improvise the ISS by including all the serious injuries with AIS greater than 2.55 Head and torso injuries are given more weightage than the rest of the injuries. All serious injuries are divided into four categories:













Category A: Head and spinal cord


Category B: Thorax and anterior neck

1. The complexity of calculations has limited its use only for research purposes.

Category C: All remaining serious injuries Category D: All remaining non-serious injuries The scoring is done using Euclidean Distance Model, viz. the square root of the sum of the squares A2 + B2 + C2 + D2. AP is considered to be a better predictor of mortality than ISS but has not been widely used because of its complexity.64 Combination Indices Trauma Revised Injury Severity Score (TRISS) TRISS is a combination index which takes into consideration both the anatomical and physiological variables of an injured patient.65 It is based on the patient’s age, mechanism of injury, RTS at admission and ISS. The advent of this index has helped clinicians in identifying and comparing outcomes in severely injured patients among different institutions across the world. The key mathematical element of TRISS is the logistic function. [1] Ps = 1/ (1 + e–b), where Ps is an estimate of a patient’s survival probability; and [2] b = b0 + b1 (RTS) + b2 (ISS) + b3 (AGE); and RTS = the admission Revised Trauma Score, ISS = Injury Severity Score and AGE = 0 for age less than 55 years, or AGE = 1 for age greater than or equal to 55. The coefficients b0 to b3 are derived from major trauma outcome studies and are different for blunt and penetrating trauma. If the age of the patient is less than 15 years, the blunt coefficients are used, irrespective of mechanism of injury.

2. The limitations are similar to using GCS and ISS. These include poor assessment in intoxicated and sedated patients, not including multiple injuries at the same site, etc. 3. The comorbidities of the patient are not taken into account. International Classification of Disease Based Injury Severity Score (ICISS) The ICISS is based on the survival risk ratios (SRRs) calculated for each anatomical injury score based ICD-9 code discharge diagnosis. The calculation is done by dividing the number of survivors in each ICD-9 code by the total number of patients with the same ICD-9 code. Simple product of the SRRs for each of the patient’s injuries gives the ICISS. Although, prediction of outcomes of interest (e.g. hospital length of stay, hospital charges, utilization of resources) is better with ICISS than ISS, it has not replaced other methods of outcome analysis.66 Application of Trauma Scoring Triage Triage of the trauma patients is necessary as the resources are limited. The aim is to identify the threshold of severity scoring that would decide shifting the patient to a trauma center. This is done by the application of various field triage tools based on easy to determine physiological parameters, e.g. CRAMS, T-RTS. One major challenge lies in effective triage of patients with severe anatomical injuries whose physiological parameters remain close to normal, shortly after trauma. For the above, a field triage team developed by the American College of Surgeons (ACS) has been widely used. The ACS Field Triage System is a decision scheme describing indications for transport to a trauma center. Apart from various physiological and anatomical criteria, mechanism of injury and comorbid factors are also included (Fig. 3.2). It is a comprehensive, advanced and easy to use

Triage and Trauma Scoring 27 FIELD TRIAGE DECISION SCHEME Measure vital signs and level of consciousness Step One

Glasgow Coma Scale .......................................................................... 5 mph) impact Pedestrian thrown or run over Motorcycle crash >20 mph or with separation of rider from bike

Evaluate for evidence of mechanism of injury and high-energy impact

Initial speed >40 mph Major auto deformity >20 inches Intrusion into passenger compartment >12 inches



Contact medical direction and consider transport to a trauma center Consider trauma team alert

Step Four

• • • • • •

Age 50 Cardiac disease, respiratory disease Insulin-dependent diabetes, cirrhosis, or morbid obesity Pregnancy Immunosuppressed patients Patients with bleeding disorder or patient on anticoagulants



Contact medical direction and consider transport to a trauma center Consider trauma team alert

Re-evaluate with medical direction


Fig. 3.2: American College of Surgeons – Field triage decision scheme (Reproduced with permission from American College of Surgeons Committee on Trauma. Advanced Trauma Life Support Manual. 9th ed. Chicago, 2012)


Essentials of Trauma Anesthesia and Intensive Care

triage system. This tool has been widely used over the last 20 years.27 Trauma Registries Though trauma is a global problem, no organized system of medical reporting and record maintenance exists in majority of countries. Trauma registries do exist at national, state, local and institutional level in developed countries which aid in allocation of finances and resources at the various levels. But there are internal inconsistencies in the recording and interpretation of data.27 This often limits the use of the recorded data for epidemiological purposes. The trauma scores are standardized scores which are central to predict survival and for quality assurance. The Major Trauma Outcome Study (MTOS) had emphasized the importance of inter institutional collaboration in trauma indices.67 Since then, many standardized registries have been developed in countries, like USA, UK, Germany, Norway, etc. These registries are retrospectively analyzed for accuracy and validity and the limitations are gradually improved upon. Research Injury severity scores are used as a means of controlling the differences in the heterogeneous trauma patients. These scores tend to decrease the confounding factors and help to draw valid conclusions. TRISS is the most commonly used combination trauma score for this purpose. TRISS has been used throughout the world in this fashion and allows for a reasonably effective mechanism by which anatomy, physiology, age and mechanism of injury can be taken into account as to their influence on outcome, when some other independent variable is being studied. SCORING SYSTEM CHALLENGES Trauma severity scales, though established and indispensible part of triage, are not free of limitations. The various challenges faced are as follows: 1. There is no single tool which considers all the characteristics of the patient. Few scales take into account the mechanism of injury, age of the patient or the presence of comorbidities. 2. Difficulty in measuring GCS in intubated, sedated and paralyzed patients leads to imperfect measurement. Hence, new scores are required for such patients to accurately measure coma.

3. Inaccurate or incomplete data at the prehospital or inhospital level often leads to difficulty in calculating the scores and hence the outcome. 4. Death is the only outcome measure which is taken into account. Development of other measures is required. 5. Difficulty in measuring multiple and complex injuries. The present literature suggests that a combination of physiologic, anatomic, and select mechanistic criteria would be the best triage tool for prehospital and in-hospital triage of trauma. Since we do not have this perfect triage tool, few facts about using other tools should be remembered. Physiological tools are better predictors of mortality than anatomical tools. Certain mechanisms of injury perform better than others and comorbidities and field personnel judgment have the lowest yields. Extremes of age should be given more importance in the triage of the trauma patient. FUTURE OF TRIAGE AND SCORING SYSTEMS Trauma is a disease whose outcome is not only affected by the patients’ physiological response, but also the organizational response of the emergency services. The health burden is increasing day by day with patients expectations on a rise. The present trauma care system faces challenges and complexities at various levels. 1. A standardized trauma care system should be in place which can be applicable at various levels: ambulance service, prehospital care providers, general practitioners’ and trauma centers. The Cape Triage Group has correctly identified this problem and is trying to come up with a standardized system.68 The French SAMU (stands for Service d’Aide Médicale Urgente or Urgent Medical Aid Service) system is another example wherein there is integration of care at all levels: firemen, ambulance drivers, private practitioners and hospitals all working as a team in the emergency medical services.69 2. The present triage tools have few limitations. An ideal trauma triage tool should take into account the following criteria also: a. Age: Extremes of age have poorer prognosis. TRISS has divided the patients into two groups younger or older than 55. But, TRISS has not been validated for children.

Triage and Trauma Scoring 29

b. Presence of comorbidities: The response to injury depends on the physiological reserve of an individual. Presence of comorbidities like diabetes, hypertension worsens the prognosis. Till now, no triage tool takes into account the presence of comorbidities. c. Mechanism of injury: Though penetrating and blunt injuries are treated as separate entities, blast injuries are nowhere mentioned in any triage tool. 3. Inaccurate trauma registries. Though developing nations contribute to the maximum number of trauma patients, record keeping is practiced in only few of them. There are no regular audits or clinical meetings at the end of an event. An example of an effective audit system is TARN (Trauma Audit and Research Network) in UK.70 Around 90 NHS hospitals contribute to the audit system. It is seen as a leader in maintenance of trauma registries. SUMMARY Trauma is a complex disease process. Characterization of injury severity is crucial to the scientific study of trauma. Trauma scoring systems, though many in numbers, are not free of limitations. Ideal trauma methodology should also take into account the age, pre-injury health status and prehospital physiological data of the patients. A great deal of research work needs to be carried out in this field. As health care systems become more complex, integrated triage, prioritization and streaming systems remain the key to improving patient outcome and survival. Further research will refine the present scoring systems and improve their accuracy. REFERENCES 1. Sethi D, Racioppi F, Bertollini R. Reducing inequalities from injuries in Europe. Lancet 2006; 368:2243–50. 2. Krug E. World Report on Violence and Health: A Summary. Geneva, World Health Organization, 2002. 3. Ronald VM. Trauma and trauma care: General considerations. In: Michael WM, Keith DL, Gerard MD, Ronald VM, et al., eds. Greenfield’s Surgery Scientific Principles and Practice, 4th Edition. Philadelphia: Lippincott Williams and Wilkins; 2010. 4. Lerner B, Ronald M. The golden hour: Scientific fact or “Medical Urban Legend”. Acad Emerg Med 2001; 8:758–60. 5. Sasser S, Varghese M, Kellermann A, Lormand J. Prehospital trauma care systems Geneva: World Health Organization; 2005. 6. Jonathan LB, Maerk C, Jeanne MA, Kim MF, et al. Evidence for and impact of selective reporting of trauma triage mechanism criteria. Acad Emergency Med 1996;3:1011–15.

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39. Narayan RK, Greenberg RP, Miller JD, et al. Improved confidence of outcome prediction in severe head injury. J Neurosurg 1981: 54;751–62. 40. Winkler JV, Rosen P, Alfry EJ. Prehospital use of Glasgow Coma Scale in severe head injury. J Emerg Med 1984;2:1–6. 41. Trauma scoring. Available from (Accessed on 17-11-2014). 42. Champion HR, Sacco WJ, Hannan DS, et al. Assessment of injury severity: The triage index. Crit Care Med 1980;8:201–08. 43. Sacco WJ, Champion HR. The trauma score as applied to penetrating injury. Ann Emerg Med 1984;13:415–18.

58. Osler T. Injury severity scoring: Perspectives in development and future directions. Am J Surg 1993; 165:43S–51S. 59. Osler T, Baker SP, Long W. A modification of the Injury Severity Score that both improves accuracy and simplifies scoring. J Trauma 1997;43: 922–25. 60. Lavoie A, Moore L, LeSage N, Liberman M, Sampalis JS.The New Injury Severity Score: A more accurate predictor of in-hospital mortality than the Injury Severity Score. J Trauma 2004;56:1312–20. 61. Sullivan T, Haider A, DiRusso SM, Nealon P, Shaukat A, Slim M. Prediction of mortality in pediatric trauma patients: New injury severity score outperforms injury severity score in the severely injured. J Trauma 2003;55:1083–87.

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67. Champion HR, Copes WS, Sacco WJ, Lawnick MM, Keast SL, Bain LW Jr, et al. The major trauma outcome study: Establishing norms for trauma care. J Trauma 1990; 30:1356–65.

64. Frankema SP, Steyerberg EW, Edwards MJ, vanVugt AB. Comparison of current injury scales for survival chance estimation: An evaluation comparing the predictive performance of the ISS, NISS and AP scores in a Dutch local trauma registration. J Trauma 2005; 58: 596–604. 65. Boyd CR, et al. Evaluating Trauma Care: The TRISS method. J Trauma 1987; 27:370-78.

68. Gottschalk SB, Wood D, DeVries S, Wallis LA, Bruijns S. The cape triage score: A new triage system South Africa. Proposal from the cape triage group. Cape Triage Group. Emerg Med J 2006;23:149–53. 69. Available from (accessed on 03-11-2014). 70. Lecky F, Woodford M, Edwards A, Bouamra O, Coats T. Trauma scoring systems and databases. Br J Anaesth 2014;113:286–94.


Essentials of Trauma Anesthesia and Intensive Care



Approach to a Trauma Patient and Anesthetic Considerations Babita Gupta


Prompt recognition and appropriate management of immediate life-threatening injuries by following systematic approach of evaluation and resuscitation during pre-hospital transport, in emergency room (ER) and operating room (OR) can have far reaching beneficial consequences. An anesthesiologist has a vital role to play during the entire journey of the patient right from ER to OR and many times to intensive care unit (ICU).

With the increasing burden of trauma patients globally, an anesthesiologist will face the anesthetic management challenge of this disease either in acute trauma setting or when the patient is shifted from ICU to OR for definitive surgery, operation being performed as a sequel to damage control surgery or surgical treatment of complication.

The priorities as described in the Advanced Trauma Life Support (ATLS®) course being conducted under the auspices of American College of Surgeons are: Airway with cervical spine control, breathing and ventilation, circulation with hemorrhage control, disability and environmental control, with simultaneous resuscitation.

Transfusion therapy with packed red cells and blood products along with surgical hemostasis or radiologic intervention to control source of bleeding are the cornerstones of trauma management.

Resuscitation efforts should be directed towards prevention and treatment of lethal triad, i.e. hypothermia, acidosis and coagulopathy.

Damage control resuscitation approach should be employed which comprises hypotensive resuscitation, hemostatic resuscitation and damage control surgery.

Massive transfusion protocols should be employed in each trauma center according to the resources available.

Adjunctive therapies which can assist in resuscitation are tranexamic acid, vasopressors and calcium.

INTRODUCTION In 1970s, the development of trauma systems in United States and eventually in all developed countries changed the approach to a trauma patient. The urgent need to approach and manage these patients in a standardized and systematic way was emphasized. The development of trauma systems and trauma centers although is in nascent stage in India, but is growing rapidly with increasing awareness at all levels of government and hospital administration. The continuum of care of a trauma patient starts right from the time of injury, continues in the emergency room (ER) and operating room (OR) and many a times extends in the intensive care unit (ICU). Prompt

recognition and management of immediate life-threatening injuries and skilful decisions during pre-hospital transport, in ER and OR can have far reaching beneficial consequences. An anesthesiologist has a vital role to play during the entire journey of the patient right from ER to ICU. With the increasing burden of trauma patients globally, including India, 1-3 an anesthesiologist will face the anesthetic management challenge of this disease either in acute trauma setting or when the patient is shifted from ICU to OR for definitive surgery, operation being performed as a sequel to damage control surgery or for surgical treatment of complication. Management of trauma patients presents unique challenges to the trauma physician and even so to

Approach to a Trauma Patient and Anesthetic Considerations 33

the anesthesiologist. A trauma patient can present with multiple injuries, some of which may be occult and may have been missed during primary survey. The damage control surgery and most other primary surgeries for the trauma patient are of emergent nature. Prompt management is required for the trauma victim because 50% of mortality in this group of patients occur within the first 24 hours.4,5 R Adams Cowley introduced the concept of “Golden Hour”; interpreted as patients with major trauma had higher survival rates, if surgical intervention occurred within one hour of injury.6 He stated “there is a golden hour between life and death. If you are critically injured you have less than 60 minutes to survive. You might not die right then; it may be three days or two weeks later–but something has happened in your body that is irreparable”.7 However, there is no definitive research that validates the time frame of one hour.8 Some patients survive although treated after more than an hour, some succumb although treated immediately. The concept, though, is very important; the sooner we can get a patient with major injuries to a trauma center, the better the chances of survival. Hence, the “Golden Period” is probably a better description. There is also a description of the “platinum 10 minutes” which means no longer than 10 minutes should be spent at the site of trauma in assessing and providing basic life-support and thereafter the patient should be transported to an appropriate trauma center.9 Since there is a lack of robust pre-hospital system in our country, it would be appropriate to say that as soon as the patient arrives in ER it should be considered as platinum/golden period and treated aggressively. The Advanced Trauma Life Support (ATLS®) curriculum of the American College of Surgeons has described the prioritization of trauma care and developed a systematic approach of evaluation and resuscitation for this purpose.10 These principles of trauma management stand out as pillars in trauma system design; understanding which an anesthesiologist has to determine his optimum role in the multispecialty effort for achieving the goal of patient survival. As a member of the emergency team, the anesthesiologist has to extensively follow the systematic approach of evaluation as enumerated in ATLS® course along with resuscitative efforts. As an OR anesthesiologist, he may not get ample opportunity to follow all the steps as most of them would have already been accomplished and also he would not get sufficient time for doing so. However, he should quickly follow those steps of evaluation utilizing the resources that are available to him to avoid missing out any

aspect in the care of the patient. Tertiary survey will be done later; many a times in ICU by the treating physician or the anesthesiologist where he would be managing the patient as a critical care physician. It is beyond the scope of this chapter to describe initial assessment of a trauma patient in detail. This chapter enumerates the basic principles of the initial approach to a trauma patient as recommended by ATLS ® from the anesthesiologist’s perspective which would help a trauma anesthesiologist in perioperative management of the patient. Treatment of a severely injured patient requires rapid assessment and resuscitation in a systematic and prioritized manner. This approach is termed as initial assessment and mainly includes:

• • • • • • •

Preparation Triage Rapid primary survey Resuscitation of vital functions Detailed secondary survey Definitive care Tertiary survey is done at later stage and is an ongoing process to diagnose and manage injuries and their complications

PREPARATION The resuscitation bay in the ER as well as the OR should be adequately equipped with properly functioning airway equipment and should be kept at a place where it is accessible and immediately available. All monitoring devices should be checked; warm intravenous (IV) fluids and emergency drugs should be readily available. All the personnel taking care of trauma patient must wear standard protective devices which include face mask, protective eyewear, shoe cover, waterproof gown and gloves to protect themselves from communicable diseases, like hepatitis and acquired immunodeficiency syndrome. TRIAGE In a busy trauma ER, several patients with diverse type of injuries may present simultaneously. Some patients may have life-threatening injuries and some may not. Hence, it is essential to triage patients, according to the severity of injury and clinical condition of the patient. The word triage means ‘to sort’ which in ER setting categorizes the patients into


Essentials of Trauma Anesthesia and Intensive Care

emergent, urgent and non-urgent.11 Emergent patients are the patients who are severely injured and have life-threatening conditions. These patients have the highest priority and should be managed immediately. Urgent patients have serious injuries but do not have immediate life-threatening situations. Non-urgent patients have minor injuries and can be addressed after emergent and urgent patients have been taken care of. However, it is important to reassess and retriage the patients repeatedly and manage accordingly. PRIMARY SURVEY: ABCDE APPROACH AND RESUSCITATION A rapid and efficient assessment of the vital functions of a multiply injured patient in a systematic way with establishment of treatment priorities based on their injuries and mechanism of injury are the key principles in primary survey. This process begins with the ABCDE of trauma care, which guides the identification of life-threatening situations through the initial assessment sequence of: A: Airway maintenance with cervical spine protection B: Breathing and ventilation C: Circulation with hemorrhage control D: Disability: Neurologic status E: Exposure/environmental control: Expose the patient, however, prevent hypothermia The sequence of priority is based on the fact that the abnormality which poses the greatest threat to life is addressed first. A rapid method for assessment of the A, B, C and D includes verbal communication with the patient, and asking his name and mechanism of injury. An appropriate response ensures that airway is not in immediate jeopardy, breathing is not severely compromised, cerebral perfusion is intact and there is no major decrease in level of consciousness. A patient who fails to respond or gives an inappropriate response suggests an altered level of consciousness, airway and ventilatory compromise or both and indicates further evaluation. Airway with Cervical Spine Control Establishing and maintaining a patent airway remains the first priority in management of trauma patient since hypoxia can cause irreversible brain injury and death within minutes. The airway should be assessed to ascertain patency. Assessment for airway obstruction includes inspection for foreign bodies and facial, mandibular, or tracheal/laryngeal

injuries which result in airway obstruction. The clinical manifestations of compromised airway include choking, apprehensive appearance, refusing to lie flat, noisy breathing, inspiratory and expiratory stridor, labored breathing, use of accessory muscles (suprasternal and intercostal retraction, flaring nostrils), anxiety and obtundation. It is important to remember that agitated and abusive patient might be hypoxic and obtundation of reflexes could be due to hypercarbia and should not be mistaken for drug/alcohol intoxication. Cyanosis and loss of consciousness develop as hypoxia worsens and are late signs; action must be taken before these manifestations develop. Pulse oximetry should be used early in the airway assessment to detect inadequate oxygenation. Airway obstruction needs immediate action, starting with simple maneuvers, like chin lift or jaw thrust. An appropriate sized oropharyngeal or nasopharyngeal airway may be inserted to maintain a patent airway. However, base of skull fracture should be ruled out prior to nasopharyngeal airway insertion. Foreign body, blood, vomitus or secretions should be suctioned out with a wide bore rigid suction cannula. Supplemental oxygen by high flow oxygen mask (12-15 L/ min should be provided to all patients. All trauma patients are assumed to be full stomach; hence it is important to anticipate vomiting and be prepared to manage the situation. Regurgitation of gastric contents in the oropharynx of patient with altered level of consciousness or obtunded reflexes poses a threat of aspiration with the patient’s next breath. Hence, immediate suctioning with a wide bore cannula and rotation of the entire patient to the lateral position should be performed. All the patients with blunt multisystem injury, especially with an altered level of consciousness or a blunt injury above clavicle should be assumed to have cervical spine (C-spine) injury unless proven otherwise. Hence, in a trauma setting, assessment and management of patient’s airway is always with C-spine protection and great care should be taken to prevent excessive movement of the C-spine. The patient’s head and neck should not be flexed, extended or rotated while assessing or managing the airway.12 Appropriate immobilization devices, such as semirigid cervical collar, should be used to immobilize the C-spine and manual in-line immobilization (MILS) should be accomplished, if there is a need to remove the anterior part of cervical collar for airway intervention.13 The MILS can be applied from the front or the side of the patient. During this maneuver, the healthcare personnel should support the occiput and

Approach to a Trauma Patient and Anesthetic Considerations 35

mandible with both hands to maintain neck alignment without applying traction (Fig. 4.1). The anterior portion of the cervical collar is removed prior to laryngoscopy to allow for easy intubation, application of cricoid pressure and surgical airway, if the need arises. MILS should be initiated while applying the bag and mask ventilation and as soon as the collar is removed.

Fig. 4.1: Manual in-line stabilization (MILS) being applied to immobilize the head and neck of the patient. During this maneuver, the healthcare personnel should support the occiput and mandible with both hands to maintain neck alignment without applying traction

Definitive airway is indicated based on following clinical findings:

• Airway problems: Inability to maintain an unobstructed airway with impending or potential compromise of the airway.

• Breathing problems: Presence of apnea and adequate oxygenation not maintained by supplemental oxygen by face mask.

• Disability problems: Traumatic brain injury with Glasgow Coma Scale (GCS) score < 8, requiring assisted ventilation and protection of airway from aspiration of blood and vomitus. One must always be prepared for the unanticipated difficult airway situation. Although the options included will vary according to institutional protocol and provider’s experience, a difficult airway cart comprising various size of laryngoscope blades, endotracheal tubes and bougie should always be kept ready in the ER and OR. This is

especially useful in the setting of C-spine injury, facial injury, mandibular fracture, foreign body or laryngeal/tracheal injuries. Obese patients may also have a difficult airway. The standard monitoring devices used during intubation must be present. Direct laryngoscopy following modified rapidsequence induction of anesthesia accompanied by cricoid pressure and in-line cervical stabilization is the most widely practiced and safest approach. Anesthesia and neuromuscular blockade allow the best intubating condition and are advantageous in an uncooperative and hypoxic patient when intubation is not anticipated to be difficult. Attempts to secure the airway in an awake or lightly sedated or uncooperative patient increase the risk of airway trauma, aspiration, hypertension and laryngospasm. The induction agent and neuromuscular blocker vary in a trauma patient. Etomidate or ketamine should be used in case of hypovolemia. The dose of anesthetic must be decreased in the presence of hemorrhage, down to none at all in patients with life-threatening hypovolemia. Suxamethonium remains the neuromuscular blocker with fastest onset–less than 1 minute—and shortest duration of action of around 5 to 10 minutes. Administration of suxamethonium is associated with several adverse consequences. Hyperkalemia is not seen in the first 24 hours after these injuries, and suxamethonium may be used safely for acute airway management.14 The provider must weigh the use of suxamethonium in each individual situation. There will always be specific situations in which maintaining spontaneous ventilation during intubation is the preferred technique. If patients are able to maintain their airway temporarily but have clear indications for an artificial airway (e.g. penetrating trauma to the trachea), slow induction with ketamine or inhaled sevoflurane with cricoid pressure will enable placement of an endotracheal tube (ETT) without compromising patient safety. Cricoid pressure should be applied continuously during emergency airway management to occlude the esophagus and prevent regurgitation. The cricoid pressure should be applied from the time the protective airway reflexes are abolished until ETT placement and cuff inflation are confirmed. Although the value of cricoid pressure in occluding the esophagus is debatable, it is simple to perform and may offer secondary benefits. Some recent evidence suggests that the laryngoscopic grade of view may worsen in up to 30% of patients due to cricoid pressure.15 It is appropriate that cricoid pressure be temporarily released, if this problem is encountered.


Essentials of Trauma Anesthesia and Intensive Care

Fiberoptic bronchoscopic-guided intubation is very useful in difficult airway scenario; but in trauma setting it may have a limited role especially in ER because of the urgency for definitive airway and the presence of blood in airway which obscures visibility. Alternative airway devices include the newer laryngoscopes, like the GlideScope®, C-Mac® or Bullard laryngoscope, laryngeal mask airway, i-gel or esophageal-tracheal double lumen tube which can be used in difficult airway situation. An option for urgent needle or surgical cricothyroidotomy should also be kept available. A surgical airway (cricothyroidotomy or tracheostomy) is established when glottic edema, laryngeal fracture or severe oropharyngeal bleed obstructs the airway and attempts to establish a patent airway by non-invasive route have failed. A surgical cricothyroidotomy is preferred over tracheostomy as it takes less time, is easier to perform and is associated with less bleeding than tracheostomy.16 Surgical cricothyroidotomy is achieved by making an opening in cricothyroid membrane to establish the airway. A curved hemostat may be inserted to dilate this opening and a smallsized tracheal tube (5.00–7.00 mm OD) can be inserted. A cricothyroidotomy tube is replaced with a formal tracheostomy tube when the patient is able to tolerate this procedure. Alternatively, needle cricothyroidotomy may be done as a life-saving procedure. A 12 or 14 G needle is inserted through cricothyroid membrane after stabilization of trachea with the thumb and forefingers of one hand. The skin is punctured in the midline with the cannula attached to a syringe with saline filled in it. The needle is directed caudad, applying negative pressure to the syringe. Once the cannula is in trachea, air is aspirated in the syringe. The syringe is removed and the stylet is withdrawn, while gently advancing the catheter downward. Transtracheal jet ventilation can be initiated through the cannula or alternatively oxygen tubing with a hole cut proximally can be attached to the cannula for ventilation. Breathing and Ventilation Maintaining airway patency alone is not sufficient; ensuring adequate ventilation is equally important. After the airway is determined to be unobstructed, the conditions which can compromise ventilation should be addressed. Adequate function of the lungs, chest wall and diaphragm are required for adequate ventilation, hence all the components should be evaluated. The patient’s neck and chest should be exposed and inspected to examine the jugular venous

distension, tracheal position and chest wall movement. Auscultation and percussion can also identify abnormalities which compromises ventilation. Tachypnea and decreased or absent movement of one or both hemithoraces should alert that the patient has sustained chest trauma. Asymmetrical chest movement indicates hemothorax, pneumothorax or a flail chest. The life-threatening injuries which should be identified and managed during primary survey are tension pneumothorax, flail chest with pulmonary contusion, massive hemothorax and open pneumothorax. Tension pneumothorax can compromise ventilation and circulation rapidly. Needle decompression by inserting a wide bore cannula in second intercostal space in midclavicular line should be performed immediately followed by chest drain insertion. An open pneumothorax should be managed by covering the wound by a sterile occlusive dressing on three sides followed by chest tube insertion. Massive hemothorax can be managed by chest drain insertion alone in majority of the patients. Any blood loss > 200 mL/hr for 2–4 hours or 1500 mL on insertion should be informed to the surgeon immediately.10 Flail chest with pulmonary contusion can be managed by chest tube insertion, adequate pain relief and by instituting positive pressure ventilation. Although simple pneumothorax can compromise ventilation to less extent and can be identified during secondary survey but is of clinical relevance for the anesthesiologist, if patient needs emergent surgery and intubation. Positive pressure ventilation in an intubated patient with simple pneumothorax can lead to tension pneumothorax. Hence, one should ensure placement of chest drain prior to anesthetic induction in these cases. After intubation, the adequacy of ventilation should be assessed by auscultation and capnography. In the arterial blood gas analysis, ventilation should be adequate in terms of oxygenation and carbon dioxide elimination. Circulation with Hemorrhage Control Hemorrhage that results in the reduction of circulating blood volume is the predominant cause of shock and preventable death after injury.17 Identifying that the patient is in shock, recognizing the source of hemorrhage, controlling the hemorrhage and volume resuscitation are the vital steps in the primary survey of these patients. The various causes of hypotension can be blood loss, tension pneumothorax, cardiac tamponade or neurogenic shock. However, once tension pneumothorax is eliminated, one should assume that hemorrhage is the cause of shock unless proven otherwise.

Approach to a Trauma Patient and Anesthetic Considerations 37

Signs and Symptoms of Shock The patient is assessed for signs and symptoms of shock; which mainly includes level of consciousness, color of skin, pulse rate and volume and urinary output. Level of Consciousness: Altered level of consciousness may be a sign of impaired cerebral perfusion due to reduced circulating blood volume although a conscious patient may have lost significant amount of blood. Color of Skin: Cool, clammy pale extremities with decreased capillary refill and ashen gray facial skin are helpful in establishing that the patient is in shock. Pulse: All peripheral pulses should be palpated bilaterally for rate, rhythm and volume. A rapid, thready pulse is typically seen in hypovolemic shock, although it could be present due to various other reasons. A patient with irregular pulse should be evaluated further to rule out cardiac injury. Absent central pulse not attributable to local causes is indicative of severe shock and requires immediate resuscitative measures to optimize cardiac output. Urinary Output: Low urine output indicates inadequate renal perfusion. Patients with less than 0.5 mL/kg/hour urine output may be compensating for hypovolemia. Patient may be tachypneic which may reflect an attempt to compensate metabolic acidosis. Causes of Shock Hemorrhage is the most common cause of shock in a trauma patient. The source of bleeding should be determined which may be internal or external. The patient at times may have to be log rolled to rule out penetrating injuries in the back. Exsanguinating internal bleeding may occur at four sites: chest, abdomen, pelvis and long bones; as goes the following axiom “blood on the floor and four more”. Clinical examination and imaging, i.e. chest X-ray, pelvic X-ray or focused assessment sonography in trauma (FAST) usually identifies the source of bleeding. The non-hemorrhagic causes of shock are mainly cardiogenic, obstructive, neurogenic or septic, if the patient presents late after injury. Severity of Shock and Management Hemorrhage can be graded into four classes based on clinical signs and are helpful in estimating the amount of blood lost. Class I Hemorrhage: The patient with 40%)

Need for more crystalloid




Need for blood


Moderate to high


Blood preparation

Type and crossmatch


Emergency blood release

Need for operative intervention



Highly likely

Early presence of surgeon




(Reproduced with permission from American College of Surgeons: Advanced Trauma Life Support, 9th edition. Chicago, IL, 2012) Table 4.2: Glasgow Coma Scale scoring Score

Eye opening

Best verbal response


Best motor response Obeys commands



Localizes pain




Flexed to pain


To speech

Inappropriate words

Flexion of arms with extension of legs (decorticate)


To pain

Incomprehensible sounds




No verbalization


Approach to a Trauma Patient and Anesthetic Considerations 39

should be taken to prevent secondary brain injury in a head injured patient by maintaining adequate circulatory blood volume (systolic blood pressure of around 100 mm Hg), adequate oxygenation and ventilation, normothermia and normal blood sugar levels.7,10 Early surgical stabilization of patients with unstable spinal canal injuries and incomplete neurologic deficits is also beneficial. Exposure and Environmental Control A thorough examination and assessment of the patient is performed by completely undressing the patient or cutting his garments. Body temperature may decrease with exposure of the patient, cold resuscitation fluids and loss of normal temperature regulating reflexes. Hypothermia, defined as a core body temperature below 35°C, is associated with acidosis, hypotension and coagulopathy in severely injured patients.20,21 In a retrospective study with patients, hypothermia was an ominous clinical sign, accompanied with high mortality and blood loss. The profound clinical effects of hypothermia ultimately led to higher morbidity and mortality. Hypothermic patients also required more blood products as compared to normothermic patients.22 Hence, hypothermia should be prevented throughout the resuscitation period. Once the patient has been assessed, he should be covered with warm blankets to prevent hypothermia. Warm IV fluids should be administered and a warm environment should be maintained. Adjuncts to Primary Survey and Resuscitation The adjuncts which are used during primary survey include: 1. ECG monitoring: ECG monitoring should be done in all patients. Tachycardia, bradycardia, dysrhythmia, ST segment changes should be monitored. 2. Urinary catheter: Urine output is a sensitive indicator of adequacy of resuscitation as it reflects patient’s volume status and renal perfusion. Urinary catheter should be inserted in trauma patients whenever indicated. Transurethral catheter insertion is contraindicated in patients with a possible urethral injury, which should be suspected in the presence of blood at urethral meatus, perineal ecchymosis or high riding prostate. 3. Gastric catheter: A gastric catheter should be inserted to decompress the stomach and hence decrease the risk of aspiration and also to assess for upper gastrointestinal hemorrhage.

4. Other monitoring: Pulse rate, blood pressure, oxygen saturation, respiratory rate, body temperature, arterial blood gas and serum lactate levels, should be monitored continuously. 5. Radiologic studies and diagnostic studies: Chest and pelvic X-rays are the two adjuncts which are done to provide information and guide resuscitation efforts of patients with blunt trauma. FAST and diagnostic peritoneal lavage (DPL) are useful tools to detect occult intra-abdominal bleed. Identification of the source of bleeding may indicate whether operative control of hemorrhage is indicated. SECONDARY SURVEY With the resuscitation underway after the primary survey has been completed, and the vital functions coming back to normal, the focus shifts to secondary survey. This includes detailed examination of the patient to identify all the injuries from head to toe, front and back and reassessment of all vital signs. It also includes a complete history, laboratory studies and radiological evaluation. Each region of the body is completely examined and any injury missed in earlier assessments is diagnosed and managed accordingly. A complete neurologic examination including a repeat GCS score determination is performed during the secondary survey. Diagnostic studies and interventions are performed depending on the findings of secondary survey. Patient’s history should include the mechanism of injury, previous medical illness, current medications, allergies and tetanus immunization. AMPLE mnemonic is useful for this purpose, i.e. Allergies, Medications currently used, Past illness/Pregnancy, Last meal and Events/Environment related to the injury. If mechanism of injury cannot be obtained from patient, then family person or attendant should be consulted. Mechanism of injury has a great bearing on the pattern of injury. The direction and force of injury helps in prediction of injuries. Injuries may be blunt or penetrating; thermal, chemical or radiation injury may also be involved. Physical examination from head to toe should exclude occult injuries. Laceration or contusion or evidence of fracture on scalp and other parts of the body should be ruled out. Raccoon eyes (periorbital hematoma) and Battles ear (retroauricular hematoma) signify underlying basilar skull fracture. Placement of nasogastric tube should be avoided in patients with nasal bone fracture or fracture of base of skull. Airway injury, burn patients and maxillofacial injury


Essentials of Trauma Anesthesia and Intensive Care

patients may require elective intubation. Chest, abdomen, perineal area, rectum and extremities should be systematically examined. Patient should be logrolled to examine the back for spine injury (Fig. 4.2). Per rectal examination is also performed at this time. Logrolling also gives an opportunity to remove the spine board. The spine board must be removed as soon as the patient has been transferred on a firm trolley, as prolonged use can lead to pressure ulcers. Laboratory studies should be minimal which include complete blood count, electrolytes and blood glucose level. In patients with hypovolemia, blood grouping, renal function tests and coagulation profile are essential and should be done during secondary survey. Other blood tests vary according to the type of injury, like the liver function tests

and serum amylase level. Arterial blood gas analysis should be done to confirm the adequacy of ventilation and metabolic balance. Radiological evaluation is done as the primary survey is being carried out. In case of head injury, CT scan is essential. CT scan of spine is often helpful to rule out C-spine injury. CT scan of chest and abdomen is done in multiple blunt trauma cases or as required by injury pattern. Whole spine injury may be ruled out in these scans. Chest radiographs in upright position may be done to look for pneumothorax, hemothorax, mediastinal widening, and fractures and to confirm chest tube position. FAST is done as screening method for blood in abdomen or pericardial cavity. In equivocal cases or when patient is stable, CT scan of abdomen is confirmatory. Cystogram or urethrogram may





Fig. 4.2: Examination of back by logrolling the patient (a) One person at the head end maintains manual in-line stabilization (MILS) of the head and spine to immobilize the cervical spine, while two persons support the torso of the patient by crossing their hands (b) The fourth person examines the back and slides out the spine board, while the other three persons logroll the patient at the direction of the person at head end (c) The fourth person removes the spine board (d) The patient is turned back supine while applying MILS and supporting the body

Approach to a Trauma Patient and Anesthetic Considerations 41

be required, if bladder or urethral injury is suspected. Radiograph of extremities should be done on the basis of physical examination. Indications for urgent or emergency surgery may also arise during the secondary survey. The presence of a limbthreatening injury as a result of either vascular compromise, compartment syndrome, or a severely comminuted fracture is one such indication. Although the life-threatening issues must be addressed first, patient with a pulseless extremity, compartment syndrome, near-amputation, or massively fractured extremity must go to the OR as early as possible. Patients with compound fracture, extensive soft tissue injury, perforation of bowel are also candidates for urgent surgery as any delay in operative intervention increases the chances of systemic infection. The anesthesiologist may find the secondary survey useful in the preoperative assessment, if the patient is otherwise stable starting with the history, quick physical examination and review of the laboratory and radiological investigations. TERTIARY SURVEY When a patient arrives in the intensive care unit (ICU), the primary and secondary surveys would have been completed, however, it is essential to repeat the primary and secondary surveys on admission to ICU as 10% of injuries may have been missed during initial assessment. Further assessment at this time called tertiary survey should also be performed. It includes:

• Reviewing the anatomical injuries and physiologic disturbances

• Re-examining the patient for missed injuries and new complications

• Reviewing the imaging • A more detailed assessment with clinical evaluation supplemented with intensive care monitoring The aim is to identify and treat physiologic derangements which extend beyond the ABCDE approach and mainly include: Respiration: Maintaining oxygenation and ventilation. Circulation: Maintaining hemodynamic stability and tissue perfusion. Nervous system: Preventing secondary brain damage. Pain relief: Providing adequate analgesia and sedation. Metabolic control: Maintaining blood sugar levels and correction of electrolyte disturbances.

Nutrition: Initiation of early enteral feeding or parenteral nutrition. Host defence: Prevention of infection and treatment of sepsis. Abdominal issues: Diagnosing and managing abdominal compartment syndrome with conservative treatment or surgical intervention. Musculoskeletal system: Diagnosis and treatment of complications associated with musculoskeletal trauma, such as compartment syndrome, rhabdomyolysis and fat embolism syndrome. GENERAL ANESTHETIC CONCERNS AND MANAGEMENT An anesthesiologist may face the challenge of providing anesthesia services to a hemodynamically unstable patient who has arrived from ER for emergency exploration and sometimes from ICU for definitive surgery, treatment of complications or as a continuation of damage control surgery (pack removal). Sepsis being the leading cause of complications and death in trauma patients, open injuries should be thoroughly debrided at the earliest and closed, if appropriate. This group of patients will require urgent surgery as they are the candidates for potential systemic infection. Providing anesthesia to a multiply injured patient presents with unique set of problems. Most of the emergency and urgent cases present during odd hours when more experienced anesthesiologist might not be available. The limited time precludes a detailed preanesthetic assessment and preparation. History of last meal taken by the patient, associated comorbid diseases, allergies, genetic disorders, previous surgeries or medications and prior administration of anesthesia might be unavailable. One may encounter anticipated or unanticipated difficult airway in a trauma situation. Risk of aspiration is also a concern as these patients are mostly full stomach or may be intoxicated or unconscious. Apart from providing anesthesia in OR, services of anesthesiologist may also be required for diagnostic angiography and embolization in radiologic suite, which may not be as well equipped for resuscitation as the OR. A trauma patient may have injuries requiring emergency surgery coexisting with injuries that can be repaired at any time or the patient may need more than one surgical procedure by more than one surgical discipline team. An anesthesiologist plays an important role in prioritizing surgical


Essentials of Trauma Anesthesia and Intensive Care

management on the basis of available resources and the patient’s response to therapy. The anesthesiologist must balance the need for early surgery against the need for diagnostic studies and/or adequate preoperative resuscitation. Some procedures may be postponed until the patient is more stable. Damage control surgery should be employed in the severely injured patient presenting with severe hemorrhagic shock, signs of on going bleeding and coagulopathy.23 Additional factors that should trigger a damage control approach are hypothermia, acidosis, coagulopathy, inaccessible major anatomical injury, or concomitant major injury outside the abdomen. Preoperative Evaluation



Hemodynamically unstable patients who are non-responders and rushed in OR for surgical exploration will not give any time for detailed preanesthetic assessment and laboratory investigations. Rapid preanesthetic evaluation should be performed whenever time permits with ongoing resuscitation. Pertinent questions (past anesthetic exposure and AMPLE history) should be asked, if patient is able to answer. All available radiologic investigations and laboratory values should be reviewed whenever available. Shifting the Patient All precautions should be taken to protect the spine while shifting the patient from trolley to OR table. Rigid transfer board slides (e.g. Patslides, Safeslide, Sally Roller) can be used to transfer the patient from one surface to another (Figs. 4.3 and 4.4). On many occasions, an anesthesiologist would receive patients with clamped chest drainage tube/s. The chest drain tubes are clamped while transporting the patient to prevent fluid being sucked into the pleural cavity. The clamps should be removed once the patient has been shifted on OR table. It is also essential to ensure that the collection chamber is always kept below the level of chest.


Airway Control If the patient arrives in the OR with ETT in situ, correct positioning of the tube must be verified as there is always a possibility of tube dislodgement during transportation. All attempts to convert non-definitive airway (LMA or combitube, which may have been inserted to oxygenate the patient in emergent situation by prehospital personnel or in ER) into definitive airway should be made. If the patient is not intubated, the same principles of airway management described above should be followed in the OR. Alternative

Fig. 4.3: Safeslide patient patient transfer system (a) The drawsheet beneath the patient is loosened and the receiving trolley/OR table is kept against the side of the trolley. The person transferring the patient grasps the drawsheet and tilts the patient towards himself. The receiving person slips the edge of the Safeslide patient transfer beneath the patient who is then lowered (b) The Safeslide is beneath the drawsheet. The receiving person grasps the drawsheet and draws the patient towards himself. The patient slides comfortably (c) The Safeslide is now gripped by the carry handle and withdrawn

Approach to a Trauma Patient and Anesthetic Considerations 43

not directly measured, evidence shows that lactate has a close relationship to base deficit and is a valuable indicator for shock.26 Base deficit and serum lactate are global markers of tissue perfusion and should be used routinely to guide resuscitation.27 Fig. 4.4: Sally roller

plans for airway control must always be ready in case of failure to intubate. Each hospital should have their own algorithm based on the fundamental principles of American Society of Anesthesiologists (ASA) difficult airway algorithm, depending on the available resources and skills. Surgical airway control should be considered in case of failure to intubate and ventilate. Hence, the presence of a surgeon is always desirable during anesthetic induction for performing urgent cricothyroidotomy or for emergency tube thoracostomy in the event of development of tension pneumothorax after initiation of positive pressure ventilation. Rapid sequence induction of anesthesia should be practiced to secure the airway. If time permits, fluid deficit should be partly restored prior to induction of general anesthesia to prevent hypotension and cardiovascular collapse. Resuscitation with fluids and transfusion should be continued throughout induction of anesthesia. IV induction agents should be administered in small incremental doses as the effect of IV anesthetics is exaggerated when injected into a hypovolemic patient.

Maintenance of Anesthesia Maintenance of anesthesia in hemodynamically unstable patients may include muscle relaxants with inhalational anesthetics titrated as tolerated. Histamine-releasing neuromuscular blocking agents, like atracurium and mivacurium, are better avoided as they can accentuate the already present hypotension. Nitrous oxide is avoided, if pneumothorax, bowel injury or pneumomediastinum is suspected. Extubation Usual extubation criteria should be followed. Hemodynamically unstable patient, elderly patient with pre-existing respiratory compromise, those who have received massive blood transfusion and patient with coagulopathy should remain intubated. The following criteria should be fulfilled prior to extubation: Mental Status

• • Intraoperative Monitoring • Standard monitoring which includes ECG, EtCO2, non- • invasive blood pressure (NIBP), pulse oximetry, temperature, and urine output should always be done in all the patients. Invasive monitoring (invasive arterial blood pressure and central venous pressure) is extremely helpful in guiding resuscitation and titrating vasopressors, however, insertion of these monitoring devices should not detract from the resuscitation itself. These invasive lines may be inserted after induction with ongoing surgical procedure, if emergent nature of surgery precludes their insertion prior to anesthetic induction. Serial hematocrit, arterial blood gases and serum electrolytes should be monitored intraoperatively to guide resuscitation. Blood viscoelastic tests, such as thromboelastography (TEG®) or rotational thromboelastometry (ROTEM®), give an accurate assessment of coagulopathy and can guide transfusion therapy.24,25 Serum lactate is an indirect measure of the oxygen debt and is an approximation of the magnitude of hypoperfusion and shock. Although

Resolution of intoxication Conscious, obeying commands Non-combative Adequate relief of pain

Airway Anatomy and Reflexes

• Adequate cough and gag reflexes present • Ability to protect the airway from aspiration • No excessive airway edema or possibility of airway compromise Respiratory Mechanics

• Adequate tidal volume and respiratory rate • Requiring FIO2 60 mm Hg Systemic Stability

• Adequately resuscitated • Small likelihood of urgent return to the OR • Normothermia, without signs of sepsis


Essentials of Trauma Anesthesia and Intensive Care

COMMONLY ENCOUNTERED INTRAOPERATIVE PROBLEMS Pulmonary Problems Trauma anesthesiologist may encounter pulmonary complications which may be attributed to direct chest trauma and lung injury or may be caused by pre-existing medical comorbidity which has been aggravated by traumatic insult. Elderly patients with underlying pulmonary disease are at higher risk of perioperative pulmonary complications as compared to healthy young adult patients. Increased airway pressure, inability to oxygenate and ventilate are the most common intraoperative pulmonary problems which an anesthesiologist may encounter in trauma setting. Increased Airway Pressure Blood, secretions, food particles or foreign bodies can obstruct the large airways and result in hypoxemia and increased peak airway pressures; plateau pressure remaining normal. Decreased pulmonary, diaphragmatic and/or chest wall compliance can also result in increased airway pressures, hypoxemia and hypercarbia. Both, peak airway pressure and plateau pressure are elevated in these conditions. Tension pneumothorax, hemothorax, intraabdominal bleed, and diaphragmatic hernia are the various causes of decreased lung compliance in an acutely injured patient. Hypoxemia Hypoxemic respiratory failure may result due to mismatch of ventilation and perfusion wherein ventilation is decreased relative to perfusion thus causing shunt effect. Conditions, such as aspiration pneumonitis, pulmonary contusion or acute lung injury (ALI), cause progressive obstruction or atelectasis and result in a decrease in the amount of oxygen available in distal airways for pulmonary capillary uptake. Pulmonary contusion caused by blunt chest trauma is independently associated with ALI, pneumonia and death.28 Even small pulmonary contusion can initiate an inflammatory cascade within 24 hours leading to increased pulmonary capillary permeability, decreased production of surfactant, alveolar collapse and predisposition to sepsis by circulating macrophage and lymphocytic function.29 Flail chest can also cause hypoxemia and lead to respiratory failure due to pain and splinting of chest. Transfusion-related acute lung injury (TRALI) is one of the causes of non-cardiogenic pulmonary edema, which results a few hours after transfusion. Signs and symptoms may appear 1 or 2 hours after transfusion with peak occurring within 6 hours.30-32

Tracheobronchial disruption can also cause hypoxemia due to inadequate ventilation as most of the tidal volume is lost through the rent. Persistent air leak in the chest drain system should arouse the suspicion of tracheobronchial tree injury. Hypercapnic Hypoxemia Hypercapnic hypoxemia may result when ventilated portions of the lungs are not perfused by pulmonary blood flow producing dead space effect. Increased dead space ventilation may occur in hypovolemia, pulmonary embolism, fat embolism, poor cardiac output or when the regional airway pressure is relatively higher than the regional perfusion pressure produced by the pulmonary blood flow in that area. Several related causes and disease processes often combine and act in concert or synergistically to compound respiratory failure. For example; a multiply injured patient might have increased airway pressure, hypoxemia and hypercarbia due to coexisting blockage of large airway with blood clots, pulmonary contusion with hemothorax and associated intra-abdominal bleed compounding the decrease in lung compliance. Management of Pulmonary Problems Appropriate steps for management should be initiated to maintain adequate oxygenation and ventilation and should be directed towards treating the cause. The circuit and ETT patency should be checked in case of high airway pressure. Bronchoscopic suction should be done to remove aspirated blood and secretions (Fig. 4.5). In the event of complete

Fig. 4.5: Bronchoscopic view of blood clots in the endotracheal tube, blocking the lumen of the endotracheal tube (ETT) and was the cause of high airway pressure and hypoxemia

Approach to a Trauma Patient and Anesthetic Considerations 45

blockage of ETT with blood clots causing hypoxemia, the ETT should be removed and replaced with a new appropriate sized ETT (Fig. 4.6). Tube exchange catheters can be used,

considered to develop over time, usually hours33 due to dilution and consumption of coagulation factors, hypothermia and acidosis. Early trauma-induced coagulopathy (ETIC), defined by prolonged prothrombin time (PT) upon hospital admission, is a new paradigm of trauma-induced coagulopathy as an early and primary event. 33 Three retrospective trials identified a prolonged PT, which occurs early after trauma in up to 25% of patients, as a predictor of mortality.34-36 Management

Fig. 4.6: The lumen of the endotracheal tube (ETT) blocked with blood clots in a multiply injured patient. The ETT was removed and replaced with a new ETT

if the intubation is anticipated to be difficult or has been documented to be difficult during initial attempts. Tension pneumothorax should be managed with needle decompression followed by chest drain insertion. N2O should be avoided in patients with suspected pneumothorax as it will expand the pneumothorax. Inhaled bronchodilators may relieve bronchospasm, if present. In case of development of auto-PEEP with hypotension, disconnecting the ventilator from the patient temporarily may be attempted to allow the trapped gas to escape. If the blood pressure and plateau pressure improves, auto-PEEP is the likely cause. The flows should be increased provided the plateau pressure is maintained 40%

Pulse rate




Systolic BP



Pulse pressure

Normal / ↑

Respiratory rate





Urine output (mL/hr)





Mental status

Slightly anxious

Mildly anxious

Anxious and confused

Confused and lethargic

Fluid replacement



Crystalloids and blood

Crystalloids and blood

Adapted with permission from American College of Surgeons: Advanced Trauma Life Support, 9th edition, Chicago, IL, 2012).

Pathophysiology and Management of Shock

confusion, hypotension, tachycardia (HR >120/min), tachypnea (RR 30–40/min), decreased capillary refill and decreased urinary output. Bleeding of more than 2000 mL causes Class IV hemorrhage and is a life-threatening situation. The patient presents with significant decrease in blood pressure, marked tachycardia, tachypnea, decreased capillary refill, very narrow pulse pressure, decreased level of consciousness and minimal or absent urine output. Cause of Shock Patient’s history and careful physical examination are essential to determine the cause of shock. Selected additional tests, such as X-ray chest, X-ray pelvis and focussed assessment sonography in trauma (FAST) or diagnostic peritoneal lavage (DPL) are helpful in providing confirmatory evidence for the cause of shock. Hemorrhage being the most common cause of shock in trauma patients, the potential sites of blood loss should be quickly assessed. It is easy to remember the pneumonic ‘One on the floor and four more’ i.e.: 1. Floor: External bleeding 2. Chest 3. Abdomen 4. Pelvis and retroperitoneum 5. Long bones It is important to remember that isolated traumatic brain injury does not cause shock till terminal stage. Hence, if a head injured patient presents with shock, other causes of shock and source of bleeding should be searched and ruled out. MANAGEMENT OF SHOCK It can be broadly considered under two headings: in the field and in the hospital. In Field Resuscitation It involves certain preparatory steps prior to actual intervention and management, such as:

• Calling for help: Call up for an ambulance or a means of transport to carry the patient to the definitive trauma care center

• Triage: Sorting out or prioritizing the patients. (Decision as to which patients need to be transported to trauma center)


• Communicating with the trauma center • Basic life support at site • Transporting the patient The goal of the prehospital trauma care should be:

• To promptly identify the source of bleeding and control it by external pressure

• To rapidly transport the patient to the trauma center; and

• Resuscitate the patient to maintain mental status and peripheral pulses Should Patients be Stabilized on the Scene or Immediately Shifted to Trauma Center? There is difference in opinion on whether to stabilize the patient at the site of accident (field stabilization i.e. stay and play) or shift the patient as soon as possible to the nearest trauma center after minimum treatment (scoop and run).20 Though the first method gives more comprehensive care at the site, it also delays the transfer to the trauma center. The answer would depend on how well organized and efficient the emergency medical service (EMS) is, whether there is dedicated transport vehicle available, distance from the nearest trauma center with all facilities, communication network to contact the nearest trauma center to intimate about the transfer of the patient and government policy and protocols. If the distance to the definitive trauma care is less than one hour, it is prudent to hurry the patient to the hospital without any treatment offered in the field. It has been found that the patients rushed to the trauma center without spending time on site for any intervention or stopping at an intermediate care center do better than those in whom resuscitation is attempted at the scene. Pre-hospital interventions beyond basic life support are not effective and have proven detrimental to the victim.21 The number of pre-hospital procedures was identified as the sole independent predictor of mortality. For each procedure, the patients were 2.63 times more likely to die before hospital discharge.22 This was evident in Vietnam war where many battlefield injury patients could be saved because of dramatic reduction in transit time.23 Triaging severely injured patients to hospitals that are incapable of providing definitive care is associated with increased mortality. Attempts at initial stabilization at non-trauma center may be harmful.24 Many places adopt an integrated approach where the patient is transported to the definitive trauma care as early as possible after limited primary care on the scene and additional care


Essentials of Trauma Anesthesia and Intensive Care

provided in the ambulance. If the bleeding can be controlled externally and if the evacuation time is expected to be less than an hour, it is safer to take the patient to trauma center directly without spending time on securing IV line at scene. Attempts at venous cannulation should not delay the transfer or distract the rescuer from keeping the airway patent. When hemorrhage is not controlled, the fluid therapy should be targeted to keep radial pulse palpable. It is usually required, if the blood pressure is less than 80 mm Hg.25 Patients with traumatic brain injury benefit from early volume resuscitation.26 The application of tourniquet is acceptable in prehospital setting to stop life-threatening bleeding in cases of amputation injuries or open extremity, when other measures have failed to control bleeding. However, it must be released periodically to avoid prolonged ischemia and tissue necrosis. In Hospital Resuscitation On arrival of the patient in the emergency department, the primary ABCDE protocol of trauma care must be followed. Once a patent and protected airway has been established with cervical spine protection and adequate ventilation and oxygenation have been ensured, every attempt to control the bleeding and replace the volume should be made. The control of hemorrhage can be achieved by direct pressure on the external bleeding site, tourniquets, external fixator for the long bones, pelvic binders and if required angiographic control or surgical control of bleeding in operation room (OR). Vascular access should be established early as the veins can collapse at later stage as hypovolemia progresses. This is achieved by inserting two large bore (minimum 16 G) short peripheral cannulae. These cannulae allow rapid infusion of fluid. Blood is collected for blood grouping, crossmatching, biochemistry, drug and toxin levels and blood gases as soon as cannulation is done. Cannulating a central vein is time consuming, requires expertise and may require elaborate positioning of patient. It should be deferred till initial stabilization of patient and availability of expert help. In children less than six years, intraosseous route proves useful and practical in absence of visible veins.2 If peripheral veins are inaccessible in adults, central venous catheterization using Seldinger’s technique or peripheral venotomy can be done. Ultrasound-guided central venous catheterization is associated with high success rate and fewer complications than being performed without ultrasound guidance. Early or Delayed Fluid Resuscitation The terms ‘early and delayed’ do not refer to the actual

time course but refers to whether fluid resuscitation is carried out prior to achieving hemorrhage control or following it. Some researchers describe early aggressive fluid resuscitation potentially harmful as fluid therapy in absence of hemorrhage control will cause transient increase in blood pressure, dislodging the soft thrombus (popping off the clot) and increasing blood loss further.27-30 They recommend delayed fluid resuscitation or controlled hypotension which targets fluid resuscitation to maintain systolic blood pressure of 70 mm Hg.31 Bickell et al. studied effects of immediate and delayed fluid therapy in 598 patients of penetrating torso injury.32 In one group the fluid administration was delayed till patient reached OR while the others received standard 2 L crystalloids. Seventy percent patients survived till discharge in delayed resuscitation group while 62% from immediate group survived. The complication observed in patients who survived in the postoperative period was 55 out of 238 patients in delayed resuscitation group (23%) and 69 of the 227 (30%) in the immediate resuscitation group (p=0.08). They concluded that, in hypotensive patients with penetrating torso injury, delay of aggressive fluid resuscitation until operative intervention improves the outcome. However, the study had limitations; it was a single center trial and stratification was not performed to identify patient who would benefit from delayed therapy. Moreover, the response at the trauma scene and trauma center intervals were around 8 minutes and 70 minutes, respectively. Extrapolating the results of the study in Indian setup, where the prehospital system is practically non-existent remains questionable. Another study conducted at a major trauma center, recruited 90 young adults with penetrating (n=84) or blunt (n=6) trauma with at least one systolic blood pressure reading below 90 mm Hg.33 The patients were randomly assigned into low goal mean arterial pressure (LMAP) of 50 mm Hg or high goal MAP (HMAP) of 65 mm Hg. Patients in the LMAP group had lower postoperative mortality (6 versus 10 deaths), received fewer blood products (1594 mL versus 2898 mL) and did not develop coagulopathy or MODS compared to 7 cases of coagulopathy and 2 cases of MODS in the HMAP group. However, there was no statistically significant difference in both the groups in overall mortality at 30 days. The key principle of fluid resuscitation is to balance the goal of hypoperfusion with the risks of re-bleeding by accepting a lower than normal blood pressure. The recommendations given by expert opinion and based on the results of various studies suggest titrating fluid administration to restore consciousness, palpable radial pulse, and a systolic

Pathophysiology and Management of Shock

blood pressure of 80–90 mm Hg until definitive control of bleeding can be achieved. Fluid administration should be aimed to a systolic blood pressure of at least 100 mm Hg in patients with hemorrhagic shock with traumatic brain injury. This resuscitation strategy serves as a bridge to definitive surgical control of bleeding and is not a substitute for it. How Much Volume Should be Infused? It is a known fact that anemia is tolerated well than hypoperfusion. Since hemorrhage remains the main preventable cause of trauma-related death, the initial concept was to give large amount of crystalloids to rapidly restore the circulating volume to normal or even supranormal levels, as soon as the basic trauma ABC has been taken care of.34 The side effects of this aggressive fluid therapy became evident subsequently, more aptly referred as ‘resuscitationinjury’. As discussed earlier, trauma involves increased capillary permeability producing leaky capillaries and loss of membrane pump integrity driving fluid inside the cell causing cellular swelling. Large volumes of fluid will further increase cell edema pressing on the capillaries, compromising perfusion, eventually producing acidosis. Development of secondary abdominal compartment syndrome is directly attributed to large volume crystalloid administration.35 Aggressive fluid therapy also leads to fulminant pulmonary failure reported during Vietnam war as ‘DaNang lung’ or ‘acute respiratory distress syndrome’. Fluids also cause increased blood pressure and popping off the soft clot and thus increased bleeding, dilution of red blood cells (RBCs) reducing the oxygen carrying capacity, coagulopathy by diluting the clotting factors and hypothermia because of large volume fluid resuscitation perpetuating the ‘bloody vicious cycle’ of trauma. In addition, there is flaring up of immune response and development of ARDS like picture. Hence the current understanding is that the fluid therapy should be started while the hemorrhage control is achieved; 1–2 L of warm, isotonic fluids should be infused rapidly in a patient who is hypotensive to get palpable radial pulse and improved mentation. If required, rapid infusion sets are used. In children, the fluid volume should be 20 mL/kg. Response to Resuscitation While administering initial resuscitation fluids, response to the resuscitation should be judged after small aliquots (250– 500 mL) of fluid are infused as that is a guiding factor for subsequent therapy. Based on the response, the patients can be categorized as:


i. Rapid responders: After initial bolus, the hemodynamic parameters become normal and remain so. In them, the blood loss is less than 20% and there is no ongoing blood loss. They require continued monitoring and maintenance fluids. ii. Transient responders: After fluid bolus, there is transient improvement in parameters but again patient’s condition deteriorates. This indicates either inadequate resuscitation or ongoing blood loss. Both issues must be addressed promptly. They have lost up to 40% of blood volume, require blood and surgical or angiographic control of bleeding. iii. Non-responders: Some patients may fail to respond to both fluids and blood. They have had massive blood loss (>40%) which is not yet controlled. Other causes of failure of treatment must also be considered, such as tension pneumothorax, cardiac tamponade or primary pump failure. Which Fluids Should be Used? There is a constant controversy regarding whether to infuse crystalloids or colloids to trauma patients. To decide this, one has to understand the pathophysiology of fluid loss in trauma. Vascular compartment is deficient as there is blood loss and along with RBCs, there is loss of coagulation factors, electrolytes and plasma. Because of the tissue injury, the interstitial compartment is deficient, some fluid is taken up by the cells and some moves inside the vascular compartment to compensate for the blood lost. It is also important to know the fluid dynamics in all three compartments of the body to decide the type of fluid to be given. The fluid administered should replace the interstitial fluid loss and should have a similar composition, should not only replenish the vascular compartment but remain there for sufficiently long period. It should not be hypotonic as it will further exaggerate the cellular edema. Crystalloids The crystalloids having composition similar to interstitial fluid would be the ideal fluids. They are cheap, easily available, with no allergy potential, no risk of transmission of infection and have the necessary electrolytes. Once infused, they get rapidly distributed throughout the extracellular space with only 20% remaining inside the vascular space. However, they lack the oxygen carrying capacity and the coagulation capacity. The most widely used


Essentials of Trauma Anesthesia and Intensive Care

crystalloids are Ringer lactate (RL) and normal saline (NS) as they are isotonic with plasma. NS was the first to be discovered and used. But it has certain disadvantages. Generally, larger volume of NS is required to maintain the target mean arterial pressure (MAP) causing undesirable expansion of peripheral compartment.36 It is also associated with dilutional coagulopathy and non-ionic gap hyperchloremic acidosis.37 The recommendations given by ATLS® include RL as the fluid of choice in hemorrhagic shock. The lactate moiety gets converted to pyruvate or CO2 and water, provided the liver function is normal. There is release of OH– which gets converted to bicarbonate helping in buffering action against acidosis. The resuscitation fluids significantly reduce the cellular damage resulting from shock by reducing the apoptosis during shock.38 But the choice of fluid also has significant influence on flaring up of inflammatory response apparent in the form of activation of neutrophils. Trauma and hemorrhage cause activation of neutrophils which is further exaggerated by infusion of RL. Even in absence of hemorrhage, RL is known to produce neutrophil activation. 39 Chirality plays a role in the inflammatory response. Conventional RL is the racemic mixture of the D and L isomers. It is the D isomer that is responsible for inflammatory response which is reduced considerably after its removal.40 RL and blood must be administered through separate IV lines because of the risk of clot formation. Use of Hypertonic Saline in Resuscitation Hypertonic saline (HS) is a hyperosmolar solution (2,400 mOsm/L) and is available in various concentrations, such as 1.8%, 3% and 7.5%. HS may provide beneficial effect through osmotic movement of interstitial fluid into the vascular compartment and restoring it, thus enhancing the preload. It also has direct vasodilatory effect on systemic and pulmonary vessels and thus reduces the afterload. A small dose of 4 mL/kg HS suffices as it expands blood volume by 3–4 times the infused volume. The volume expansion by 7.5% HS is 10 times more than the equivalent volume of NS.41 This may make HS the initial fluid of choice on battlefield as usually only 250 mL would be required. It also improves regional microcirculatory flow, controls intracranial hypertension by reducing the cerebral volume, and stabilizes arterial blood pressure and cardiac output. It has positive inotropic effect on myocardium. 42 It causes immunomodulation by restoring the T-cell function which is depressed by hemorrhage. It also improves regional blood

flow to renal and mesenteric vascular beds and reduces injury to liver and lungs.43 The main side effect of HS is high sodium load causing hypernatremia and hyperchloremia. There is also dose-dependent risk of increased bleeding, the risk being minimum, if the dose used is 1mg/kg.44 The volume expansion effect is short lived and can be extended further by addition of dextran solution. The common preparation is HSD 7.5% with 6% dextran-70. Since the volume used is very small, it is very convenient in the pre-hospital setting. Although few clinical trials have shown improved outcomes, other studies failed to show improved survival. More studies are required to establish the beneficial role of HS. Should Colloids be Used in the Resuscitation in Trauma? Colloids have the benefit that they remain in the vascular compartment for a longer period and not only restore but expand the blood volume, the volume required to replace the blood loss is much less than crystalloids, thus reducing the cellular edema. They are responsible for maintaining colloid osmotic pressure of the plasma. The shortcomings of colloids are their cost, relative non-availability, the allergic potential and their effect on crossmatching. In the initial period, the prototype of colloids was albumin. It does not cause neutrophil activation. Apart from albumin, other colloids available are plasma and synthetic colloids, like the gelatins, starches and dextrans. Gelatins are made from collagen and can be urea-linked or succinylated and have relatively low molecular weight. These compounds remain in the circulation only for a small period but have no limitation on dose. They have high incidence of hypersensitivity reaction. They have low volume efficacy, and less inhibitory effect on clot strength. Starches are the polymers of amylopectin and are of different types depending on their molecular weight and molar substitution. Hydroxyethyl starch (HES) is a high molecular weight starch solution having a high (0.7) molar substitution and remains in the circulation for almost 24 hours. It is known to cause coagulopathy. The dose is restricted to 20 mL/kg. Pentastarch is a medium weight homogenous HES solution with 0.5 molar substitutions that plugs off the leaky capillaries in inflammatory state.45 It has a plasma half-life of six hours. In patients with hypocoagulability, tetrastarch is a suitable volume expander due to its high safety index and volume expansion. Tetrastarch in balanced salt solution should be preferred over saline-based solution.46

Pathophysiology and Management of Shock

There is controversy whether to give colloids in the initial resuscitation. In trauma, there is exaggerated permeability of the vascular endothelium. This can cause egress of large molecules, like albumin, from the capillaries. There are many studies comparing the crystalloids with colloids for trauma patients. Most of them concluded that the use of colloids is associated with a trend towards increased mortality and that trauma patients should continue to be resuscitated with crystalloids.47,48 The landmark study was the SAFE study comparing normal saline with 4% albumin in intensive care unit (ICU) patients. All the parameters, like duration of ICU stay, hospital stay, pulmonary edema, mechanical ventilation and mortality at 28 days, were comparable in both the groups. They concluded that both the resuscitation fluids should be considered equivalent. It was also noticed that the colloid to crystalloid fluid requirement was in the ratio 1:1.4 rather than conventional 1:3.49 In the Cochrane review published in 2009 and again in 2013, it was concluded that there is no evidence from the various randomized controlled trials that resuscitation with colloids reduces the risk of death in patients of trauma. Since they do not improve survival and are considerably more expensive, their use is not justified.50,51 Blood and Blood Products in Trauma As discussed earlier, trauma involves loss of blood and depletion of interstitial fluid. Blood and blood products form a part of balanced resuscitation where limited volumes of crystalloids are infused in the initial period till blood is available for transfusion after reaching the trauma center. Blood transfusion is likely to be required for blood loss 30–40% (Class III hemorrhage), and definitely for >40% blood loss.2,52 As anemia is better tolerated than hypoperfusion, if normovolemia is achieved, the normovolemic hemodilution produced reduces hematocrit and increases cardiac output by reduction in viscosity and afterload.53 The tissue oxygenation is flow-dependent rather than hematocrit-dependent.54 There is no fixed transfusion trigger but generally hemoglobin of less than 7 gm% would demand blood transfusion. However, many factors, such as age, presence of prior comorbidities, control of bleeding achieved and response to hemorrhage, decide the need for transfusion. RBCs form the mainstay of the treatment as loss of RBCs leads to loss of oxygen carrying capacity. Risk of systemic ischemia is reduced by maintenance of adequate hematocrit. However, transfusion of only RBCs does not suffice as there is dilution of coagulation factors because of crystalloid infusions and platelet deficiency. Prior to this, the concept


of one unit plasma for three units of RBCs was prevalent and there were no guidelines about platelet requirement. In a study conducted by Holcomb et al. in 466 massively traumatized patients, it was observed that patients who received all components of blood, viz. RBCs, plasma and platelet concentrates in the 1:1:1 ratio, along with limited crystalloid infusion had better outcomes.55 Blood products given in this ratio yield coagulation factors and platelets associated with best outcomes. 56 The exact ratio of RBC:plasma:platelets remains undetermined. Each institute should have their own massive blood transfusion protocol which has been shown to decrease mortality in various studies. Crossmatching of the group-specific blood takes minimum 45 minutes and in major trauma it may not be possible to wait till the crossmatched blood is available. This can be overcome by transfusion of group O RBCs; O negative in female patients of child-bearing age group to prevent Rh sensitization and O positive in others. This allows rapid administration of RBCs to the bleeding patient without discernible risk of transfusion related complications.57,58 Trauma centers should keep units of group O blood to take care of severely bleeding patients in shock. The fresh frozen plasma (FFP) should be group-specific and in an emergency, AB plasma can be given. One should remember not to heat the plasma as it will cause destruction of clotting factors. It should be thawed at room temperature. The platelets should not be refrigerated and continuously agitated. They should not be administered through filters, warmers or rapid transfuser systems. If administered through a blood set, it should be rinsed with saline to wash away the entrapped platelets. Massive Transfusion Protocol The term ‘massive transfusion’ is used when patient receives more than 10 units of blood in a span of 24 hours. Upon request for massive blood transfusion, packed RBCs, FFPs and platelets in fixed proportion should be delivered (usually 1:1:1). Massive transfusion of banked blood is associated with citrate load on the liver. It binds to free Ca++ and inhibits clotting and has negative inotropic effect on heart. Therefore, calcium must be administered through a separate line. Blood salvage should be employed whenever available. However, it is contraindicated in heavy contamination. Hypothermia must be prevented at any cost by use of warm IV fluids (39ºC) and using blood warmer. Blood warmer is necessary whenever blood flow rate is more than 50 mL/kg/hr.


Essentials of Trauma Anesthesia and Intensive Care

If the patient does not respond to the standard therapy, other causes of shock other than or in addition to hemorrhage must be suspected. These include tension pneumothorax, cardiac tamponade, cardiogenic shock and overzealous fluid administration causing abdominal compartment syndrome. In some patients who survive the initial hypovolemic shock, the recovery is complicated by development of sepsis and must be detected and aggressively treated using the early goal directed therapy.

• Oxygen saturation: Maintain more than 94% • Heart rate: Maintain 60–100/min • Blood pressure: Target MAP above 65 mm Hg or systolic


It was assumed that once these parameters are normalized, the resuscitation is complete. However, this assumption is far from valid since these parameters are not accurate measures of tissue perfusion. Shock causes microcirculatory failure at tissue level causing tissue hypoxia and acidosis. The depth and degree of shock gives rise to cumulative oxygen debt. Unless this debt is repaid and tissue acidosis is corrected, resuscitation is not complete.60 Hence, the end points must consider, in addition to hemodynamic parameters, other global and regional indicators of perfusion.61 Tables 8.4a and 8.4b enumerate the commonly used end points of resuscitation which may be used to guide prolonged resuscitation.

The clinical monitoring and the investigations which may be used to guide resuscitation of traumatic shock are enumerated in Tables 8.3a and 8.3b. Though it is said that shock is the result of failure of microcirculation, since long it is the macrocirculation that is targeted while monitoring shock and guiding resuscitation, since it is easier to monitor and manipulate. It is essential to remember that end points should not be targeted prior to achieving hemostasis. Table 8.3a: Clinical monitoring Pulse Blood pressure and pulse pressure Oxygen saturation (SpO2) Central venous pressure and passive leg raising test to predict response to fluid challenge Capillary refill Urine output Temperature End tidal carbon dioxide (ETCO2) Mentation Drain output/abdominal girth Cardiac output monitoring

BP 80–90 mm Hg

• Central venous pressure (CVP): Maintain between 8 and 12 mm Hg

• Mental status: Normalization of altered sensorium • Urine output: Maintain more than 0.5 mL/kg/hour

Table 8.4a: Hemodynamic parameters SBP

80-90 mm Hg Normotensive in head trauma MAP >65 mm Hg HR 60-100/min SPO2 >94% Mentation Good, follows commands Urine output >0.5 mL/kg/hr CVP 8-12 mm Hg SBP: systolic blood pressure; MAP: mean arterial pressure; SpO2: oxygen saturation; CVP: central venous pressure Table 8.4b: Global indicators of perfusion

Table 8.3b: Investigations Hemoglobin, packed cell volume Platelets, bleeding and clotting time Prothrombin time/activated partial thromboplastin time INR Blood biochemistry Serum lactate



Base deficit

170 mL/min/m2. It has been shown that attaining these supranormal values improves survival and reduces frequency of organ failure.63 The oxygen delivery can be enhanced by adding inotropes to improve cardiac output. Dobutamine would be the agent of choice as it does not cause peripheral vasoconstriction, thus reducing the afterload and off loading the heart.63 Another important manipulation required is improvement in the hemoglobin by blood transfusion. This is important especially in elderly patients and patients with ischemic heart disease. Mixed Venous Oxygen Saturation (SvO2): SvO2 more than 70% is predictor of better survival. If less than normal, it indicates that the oxygen delivery is not optimum.61 Hemodynamic Profiles CVP and pulmonary capillary wedge pressure (PCWP) as a measure of preload have limitations in critically ill trauma patients due to changes in cardiac compliance (edema, ischemia or contusion) and intrathoracic pressure (mechanical ventilation). Right ventricular end diastolic volume index (RVEDVI) has been found to correlate with CI better than CVP or PCWP up to very high levels of positive end-expiratory pressure.64 In a retrospective study by Chang et al., it was observed that maintaining left ventricle (LV) power output (LVP) more than 320 mm Hg × L/min/m2 is associated with improved survival [LVP = Cardiac index × (MAP–CVP)].65 To know these parameters, one has to resort to invasive monitoring, like pulmonary artery catheter which by itself is not without complications. However, the oxygen transport data obtained from it can be used not only to normalize but to augment cardiovascular status.66 Acid-Base Status Base Deficit: Base deficit is more accurate than arterial pH as change in pH is compensated by the body. It reflects both the ongoing blood loss and the quality of resuscitation. It can be classified as mild (2–5 mmol/L), moderate


(6–14 mmol/L) and severe (>14 mmol/L). Increasing base deficit indicates ongoing blood loss.61 Hyperchloremic acidosis of saline resuscitation adds to this. NaHCO3 has little role in correcting the base deficit. Once the peripheral circulation is restarted, the deficit regresses. Serum Lactate Levels: The normal level of lactate in blood is 120, very weak

Blood pressure




Very low

Capillary refill





Mental state





Respiratory rate





Urine output

>30 mL/hr

20–30 mL/hr

5–20 mL/hr

< 5 mL/hr

(Modified from Advanced Trauma Life Support Manual, Chicago: American College of Surgeons; 2012)

hypovolemia can result in changing a reversible early shock to irreversible multi-organ failure eventually leading to death. Though use of the traditional markers of resuscitation, like restoration of blood pressure, heart rate, and urine output, is considered standard of care,1 they have their own limitations. Hence, clinical monitoring must be supplemented with application of monitors, like cardioscope, blood pressure monitor, pulse oximetry and by assessment of measures, like central venous pressure or invasive arterial pressure with waveform and numeric data derived from various sites, like central veins, right atrium, pulmonary artery, left atrium, or peripheral arteries. Electrocardiography Even a simple electrocardiography (ECG) can reflect volume status, ischemia, pain, electrolyte disturbances or sometimes can suggest situations, like cardiac tamponade. Continuous ECG monitoring should be done in every trauma patient to monitor heart rate and rhythm which can vary drastically within a short span of time due to ongoing injury process and/or blood loss. There can be changes due to metabolic derangements, hemorrhage, structural injury to the heart itself, or brain or spinal cord injury. Moreover, in the operating room (OR), American Society of Anesthesiologists monitoring standards mandate attaching ECG,3 preferably using five electrodes to monitor multiple leads. Most commonly seen ECG change is tachycardia due to pain and anxiety. Hypovolemia further aggravates tachycardia, as the

body tries to maintain cardiac output by increasing heart rate. However, this may not be seen in extremely old patient or in presence of increased intracranial pressure. It has been observed that tachycardia does not occur in about onethird hypotensive patients.4 Bradycardia is often present in patients with head trauma or cervical spine injury. Hypovolemia may also alter amplitude of complexes during respiratory cycle as venous return differs more significantly. There can be other changes due to direct myocardial injury or other metabolic conditions. A patient with subarachnoid hemorrhage can have ST segment elevation, T wave inversion, QT prolongation or malignant ventricular arrhythmias.5 Furthermore, trauma patients are at increased risk of myocardial ischemia due to hemorrhage and high circulating catecholamines in presence of pre-existing coronary artery disease. During resuscitation with large volume fluids and blood, ECG changes, like QTc prolongation or ST-T changes due to hypocalcemia or tall peaked T waves due to hyperkalemia, may be seen. Hyperkalemia is also common in patients with crush injury and burns. Cardiac contusion may also cause rhythm disturbances. Low voltage ECG may be seen in presence of pericardial effusion. The data on cardioscope must be correlated with clinical findings to suspect certain life-threatening conditions, like pulseless electrical activity in presence of hypovolemia, pericardial tamponade or tension pneumothorax (Table 9.3).

Hemodynamic Monitoring in a Trauma Patient 135 Table 9.3: Etiologies of pulseless electrical activity (PEA) 5 Hs



Tension pneumothorax


Tamponade: Cardiac

Hyper and hypokalemia

Thrombosis: Pulmonary embolus

Hydrogen ions (acidosis)

Thrombosis: Coronary artery thrombosis


Toxins: Drug overdose

Blood Pressure Monitoring Systemic arterial blood pressure is an indirect measurement of circulatory well-being and is fairly reliable for managing the patient with acute trauma in pre-hospital as well as in emergency room settings. However, it has many shortcomings as an indicator of intravascular volume or blood flow. Blood pressure should be monitored at least every five minutes in the initial resuscitation period and intraoperatively and recorded in the monitoring chart.3 This is commonly done using either manual or automated noninvasive blood pressure (NIBP) monitoring. Manual measurement of blood pressure is highly dependent on the person checking and the equipment used. Moreover, it is cumbersome to repeatedly measure it in an unstable patient when the anesthesiologist needs to do many other tasks. Automated non-invasive instruments use oscillometry to measure blood pressure at regular adjustable intervals, freeing the anesthesiologist to perform other tasks. If a patient has sustained injury to both upper limbs, the cuff may be placed at the thigh or ankle to obtain values that correlate well with values obtained at the arm.6 Hypotension in trauma is often a late sign after hemorrhage and because the blood pressure is well maintained till about 30% of the blood volume is lost, it can provide a false sense of security to an inexperienced clinician. Numerous outcome studies have examined the prognostic value of blood pressure in survival of trauma patients. In a large review of the value of physical diagnosis in hypovolemia, low blood pressure had a sensitivity of only 33% even after a large blood loss.7 The term ‘shock index’ refers to the ratio of heart rate to systolic blood pressure and this variable may help to identify hypoperfused patients with

more subtle vital sign abnormalities. A shock index of greater than 0.9 has been found to be more sensitive than traditional vital sign analysis in identifying disease severity in presenting to emergency department, however, its value over other signs remains to be studied.8 Another major limitation about the use of NIBP as a guide to resuscitation is obtaining accurate blood pressure values during hypotension. Non-invasive oscillometric blood pressure measurement, although correlates well with the invasive arterial pressure in normal patients,9 does not accurately measure blood pressure in most trauma patients presenting with hemorrhagic shock with systolic blood pressure less than 80 mm Hg.6 These equipment often overestimate the systolic blood pressure6 and, therefore, are not considered reliable in the presence of rapidly changing blood pressure, arrhythmias, hypotension and hypertension. Prolonged use of automated devices and frequent blood pressure measurements can cause excessive venous pressures and tissue ischemia. Therefore, it is usually desirable to establish an arterial line in major trauma patients as soon as other emergent procedures have been performed. Arterial Pressure Monitoring Invasive arterial blood pressure (IBP) monitoring allows accurate ‘beat-to-beat’ continuous measurement of blood pressure and avoids need for repeated cuff inflation and deflation in major trauma patients. Therefore, early placement of an indwelling arterial catheter is recommended in all severely injured patients, especially in those with TBI in whom an accurate and immediate calculation of cerebral perfusion pressure (CPP) is necessary; those with hypoxemia or ventilatory failure who may need frequent arterial blood gas (ABG) determinations; and those patients in a state of shock. In the OR, a radial arterial catheter is indicated whenever large fluctuations in blood pressure are expected during laparotomies, thoracotomies, and craniotomies, as well as peripheral injuries with significant blood loss.10 The mean arterial pressure (MAP) is the best physiological estimate of perfusion pressure as it shows less variability than the systolic pressure. An MAP >60 mm Hg is a reasonable target for most patients. A higher target is needed for chronic hypertensive, head injured, spinal cord ischemia or pregnant patients. It is to be noted that an increase in blood pressure achieved using vasoconstrictor agents in


Essentials of Trauma Anesthesia and Intensive Care

a hypovolemic patient does not provide adequate organ perfusion and can be deleterious. It is important to realize that there is no direct relationship between the results obtained from the two methods of blood pressure measurement. Invasive arterial monitoring measures pressure whereas NIBP measurement reflects blood flow. Currently, direct monitoring of arterial blood pressure is the only scientifically and clinically validated method for realtime continuous monitoring of blood pressure. Central Venous Pressure Monitoring Central venous pressure (CVP) reflects right ventricular preload and, therefore, CVP monitoring provides a useful estimate of the volume status of the systemic circulation. The normal CVP ranges from 0 to 8 mm Hg. Any condition that causes increased intrathoracic pressure, such as pneumothorax or some types of mechanical ventilation, will increase CVP, while end-diastolic volume is acutely low (Table 9.4). Conditions that reduce contractility and cause the right ventricle to become rigid, such as pericardial tamponade and myocardial infarction, can also result in a high CVP in spite of hypovolemia. Low CVP can be due to reduced blood volume between the central compartments.11 Therefore, CVP measurement as a single absolute value is of little help to assess a trauma patient. However, as a monitor of trends, it gives information about response to fluid bolus and adequacy of resuscitation in the absence of cardiac dysfunction or other circulatory obstructions. It is essential that all measurements be taken in the same patient position for the trends to be valid. In presence of a cardiac Table 9.4: Common causes of altered CVP in trauma Conditions that increase CVP

Conditions that lower CVP


Absolute hypovolemia:


• Hemorrhage


• Dehydration

Intra-abdominal hypertension

Relative hypovolemia: • Sepsis

Pericardial tamponade

• Bowel obstruction

Mechanical ventilation with positive end-expiratory pressure (PEEP)

• Anaphylaxis • Systemic inflammatory response syndrome (SIRS) • Neurogenic shock • Vasodilator drugs

disease, the CVP becomes less reliable. Interpretation of CVP should always be correlated with clinical condition and type of trauma to determine the management. For example, a patient with pneumothorax and high CVP should be treated with release of tension pneumothorax and not with diuretics or inotropes. In acute trauma situations, to start fluid resuscitation large bore short cannulae are needed, through which later on peripherally placed central catheters can be inserted. Alternatively, if there are no contraindications, a double or triple lumen central venous catheter should be inserted through subclavian or internal jugular vein. Cardiac Output Monitoring Traditionally, normalization of vital signs, such as blood pressure, urine output, and heart rate were used as endpoints of resuscitation. Though the ‘static’ pressure-derived preload values, like arterial blood pressure and CVP, have been commonly used in the management of fluid titration, numerous studies have challenged the reliability of these indicators to accurately predict volume status.12 Besides, it is difficult to identify whether blood pressure is decreased due to reduced preload, afterload or poor contractility. Even though most common reason for inadequate cardiac output in a trauma patient is hypovolemia, empirical administration of large volumes of fluids can lead to volume overload and pulmonary edema in a critical trauma patient without actual benefit in maintaining blood pressure or tissue perfusion. If the fluid challenge does not increase the stroke volume, volume loading serves the patient no useful benefit and is likely to be harmful.12 Therefore, it is important to identify preload sensitivity of the patient. If the heart is on the steep part of the Frank-Starling curve, volume therapy increases stroke volume, and within this range, the patient will be fluid responsive (Fig. 9.1). However, if the heart is on the flatter portion of the Frank-Starling curve, stroke volume will not increase with volume therapy.11 Thus, monitoring stroke volume and cardiac output enables a physician to identify a trauma patient who may benefit from additional fluid infusion and plan the management accordingly. This data also provides insight into myocardial contractility and systemic vascular resistance. Assessment of cardiac output and stroke volume have been increasingly used as a dynamic monitoring modality for guiding fluid therapy in OR and critical care setups.

Hemodynamic Monitoring in a Trauma Patient 137

Stroke volume

Fluid non-responsive

Fluid responsive

Ventricular volume Fig. 9.1: Frank-Starling curve and preload sensitivity

Pulmonary Artery Catheterization Pulmonary artery (PA) catheter allows measurement of PA pressure, PA occlusion pressure (PAOP), cardiac output, stroke volume, systemic vascular resistance and pulmonary vascular resistance.13 Thus, it can separately assess the performance of the right and left ventricles and can identify isolated ventricular dysfunction. Traditionally, cardiac output is measured by bolus thermodilutional (TDCO) technique using a pulmonary artery catheter (PAC) placed through a central venous sheath and left atrial pressure is indirectly measured using PAOP.14 It provides information about cardiac output, left atrial pressure and left ventricular ejection fraction. The PAC is also useful for pulmonary artery oximetry to measure mixed venous oxygen saturation.10 The standard invasive cardiac output monitoring using Swan-Ganz catheter and thermodilution technique is not suitable in a trauma resuscitation area as it is invasive, expensive and impractical due to time constraints and the need to perform many diagnostic and therapeutic procedures simultaneously. Besides, many concerns are raised about the safety of the procedure in critically ill patients.15 It has inherent risk of carotid puncture, pneumothorax or hemothorax. A meta-analysis showed no positive association between use of PAC and survival in critically ill patients.16 Even in trauma patients, though there was insufficient evidence for survival benefit, it was recommended when underlying cardiovascular disease is present, when other non-invasive monitoring is inadequate or does not give

conclusive data or to potentially decrease secondary injury in a multisystem injury patient.17 In a very large data bank analysis, it was noted that trauma patients who are managed with a PAC are generally more severely injured and have a higher mortality. PAC has been found to have benefit only in severely injured patients arriving in severe shock and older patients.18 The pulmonary artery catheterization is now usually done only as an intensive care unit (ICU) procedure in selected high-risk population. As placement and use of the PAC are associated with a variety of complications, a review article recommended that every practitioner who uses the PAC not only must be familiar with aspects of its placement and long-term maintenance, but they must also be knowledgeable in interpretation and use of the hemodynamic information provided by the catheter.19 Technological advances have allowed these hemodynamic measurements using less invasive or non-invasive methods which have more clinical and practical benefits in trauma settings. Arterial Pulse Contour Analysis Using an invasive arterial cannulation, blood pressure waveforms are obtained which are used for measuring systolic, diastolic and mean blood pressures. Analyses of these arterial waveforms have been developed mathematically to calculate cardiac output. Though several concerns were raised for validity about these methods due to non-linearity, use of peripheral arteries, damping, aortic pathology and body position, most of these have been taken into account for calculating stroke volume and cardiac output in different machines.20 Various equipment based on this principle have been validated in trauma situations and found to be satisfactory to guide need of fluid therapy. FloTracVigilio (Edwards Lifesciences, LLC, USA), uses the arterial pressure waveform analysis, along with patient data, to calculate continuous cardiac output, systemic vascular resistance and the dynamic parameters of stroke volume variation. The device self-calibrates based on patient demographics and waveform analysis. It can be used with any arterial catheter in any arterial location. Pulse Contour Analysis and Dynamic Preload Indices Dynamic changes in arterial waveform-derived variables (systolic pressure, pulse pressure and stroke volume) in patients undergoing mechanical ventilation have emerged as useful techniques to assess volume responsiveness during resuscitation of trauma patients.


Essentials of Trauma Anesthesia and Intensive Care

Systolic Pressure Variation (SPV): Cardiac preload is highly susceptible to changes in intrathoracic pressure induced by mechanical ventilation. Positive pressure ventilation during the inspiratory phase reduces venous return, decreases right ventricular output, and after two or three heartbeats negatively affecting left ventricular output and stroke volume, which occurs usually in the expiratory phase. These changes are more pronounced in hypovolemia. The pulse pressure waveform reflects the changes in stroke volume occurring with positive pressure ventilation (Fig. 9.2). SPV is the difference between the maximal and minimal values of the systolic blood pressure during one mechanical breath.21 A pressure difference of more than 12 mm Hg during inspiration and expiration is indicative of hypovolemia and is considered as a threshold value for fluid responders.22 A decrease in the systolic pressure from the line of reference (∆Down) is more sensitive to predict hypovolemia.22 In a study conducted during abdominal surgery, SPV-guided treatment was associated with slightly more intraoperative fluid whereas organ perfusion and function were similar when compared with routine care.23

It has been recommended to use these dynamic parameters (SPV, ∆Down, PPV), preferentially to static parameters (CVP, PAOP) as they are highly accurate to predict fluid responsiveness. 24,25 Pizov et al. found progressive increase in SPV and PPV with progressive hypovolemia in absence of significant changes in heart rate and blood pressure.26

Airway pressure

Completely non-invasive method using inflatable finger cuff to analyze waveform and calculate stroke volume has also been used recently.29


PPmax SPmin


Arterial pressure

Fig. 9.2: Pulse pressure waveforms showing systolic and pulse pressure variation in hypovolemia during positive pressure ventilation (SPmax = Maximum systolic pressure after inspiratory peak; SPmin = Minimum systolic pressure after positive pressure respiratory cycle (during expiration); PPmax = Maximum pulse pressure after inspiratory peak; PPmin = Minimum pulse pressure after positive pressure respiratory cycle (during expiration); SPV = Systolic pressure variation represents the difference between SPmax and SPmin)

Pulse Pressure Variation (PPV): Pulse pressure is directly proportional to stroke volume and inversely related to vessel resistance. PPV is defined as the maximal pulse pressure less the minimum pulse pressure divided by the average of these two pressures. Rather than SPV it would more accurately reflect changes in stroke volume24 as it is not influenced by the intrathoracic pressure-induced changes in arterial pulse.21,25

Stroke Volume Variation (SVV): It is the percentage change between the maximal and minimal stroke volumes divided by the average of the minimum and maximum over a floating period of 30 seconds.21 A 10 to 15% variation in pulse pressure/stroke volume is predictive of volume responsiveness. 27 SVV monitoring does not require pulmonary artery catheterization and most importantly it provides a measurement of the left heart function. About 5% improvement in stroke volume can be anticipated with 100 mL of fluid bolus in adult patients, if SVV is over 9.5% as measured by pulse contour continuous cardiac output (PiCCO) technique.28 In contrast to the intermittent bolus thermodilutional method, pulse contour analysis can provide continuous cardiac monitoring and SVV measurements from the arterial pressure waves.

Trans-pulmonary Lithium Indicator Dilution and Arterial Waveform Analysis In the LiDCO system (LiDCO Limited, UK), a lithium-based dye-dilution technique is used to calibrate its pulse contour analysis algorithm. Following intravenous administration, lithium is detected by an external lithium ion sensitive electrode attached to an arterial catheter. Cardiac output is then calculated using a modified Stewart-Hamilton equation.30 This combined technology is less invasive, allowing use for longer periods of time in conscious as well as unconscious patients. However, irregular heart rhythm and use of non-depolarizing muscle relaxants interfere with the results.30 Trans-pulmonary Thermodilution and Arterial Waveform Analysis The PiCCO system (Pulsion Medical System, Munich, Germany) requires an external calibration (cold saline) for pulse contour analysis. A cold saline indicator is injected via

Hemodynamic Monitoring in a Trauma Patient 139

a central venous catheter and temperature is measured in arterial blood using a thermistor-tipped catheter. Cardiac output is calculated using a modified Stewart-Hamilton equation and by a pulse contour analysis method. The PiCCO monitor also provides global end-diastolic volume measurements of all cardiac chambers and also provides extravascular lung water measurements.31 In a large prospective, epidemiological study comparing PAC with PiCCO system, use of PiCCO was associated with higher fluid balance and less ventilator days, but the choice of monitoring did not influence patient outcome.31 Due to its invasive nature, the technique may have some practical disadvantages in an emergency situation in a trauma setting. Transthoracic Impedance Cardiography Transthoracic impedance cardiography is a non-invasive method of obtaining continuous measurements of cardiac output and central fluid volume with little expertise.32 It involves application of four sets of electrodes—two each at the root of the neck and lower costal margin. A small alternating current across is applied to the chest via topical electrodes. This current distributes primarily to blood because of its high electrical conductivity as compared with muscle, fat and air and less impedance is measured in patients in a hypervolemic or normovolemic state in comparison with hypovolemic states.33 The technology measures two types of impedances— pulsatile and baseline. Pulsatile impedance changes occur due to changing volume of blood in ascending aorta during cardiac cycle. Increased aortic flow during systole decreases the impedance as compared to diastolic phase and it directly represents left ventricular function. Baseline or ‘thoracic’ impedance is average impedance calculated from these pulsatile variations for a given period of time.33 Both these values are correlated with data from the cardioscope and cardiac output is then calculated using peak aortic flow, stroke volume and heart rate.34 Other derived parameters include cardiac index, stroke volume, systemic vascular resistance and thoracic fluid content.35 The new Cheetah NICOM (Bioreactance Technology) can monitor cardiac output non-invasively using this principle and is simple and quick. In trauma, where one needs to quickly diagnose complex injuries and rapidly make treatment decisions, such non-invasive modalities are of practical help.35,36 CO2 Elimination Based Cardiac Output Monitor ®

Non-Invasive Cardiac Output (NICO ) Monitor (Philips

Respironics, The Netherlands) measures cardiac output based on changes in respiratory CO2 concentration using partial rebreathing technique with a plastic loop connected to breathing system.37 It is non-invasive, automated and employs modified Fick’s partial rebreathing principle.38 The technique compares end-tidal carbon dioxide partial pressure (PETCO2) obtained during a non-rebreathing period with that obtained during a subsequent rebreathing period. The ratio of the change in PETCO2 and CO2 elimination after a brief period of partial rebreathing (usually 50 seconds) provides a non-invasive estimate of the CO2.12 The machine measures only pulmonary capillary blood flow and adds fraction of shunted blood by calculating Qs/Qt by using a shunt correction algorithm that uses oxygen saturation from pulse oximetry and the fractional concentration of inspired oxygen.12 It can be easily used in mechanically ventilated acute trauma patients in emergency room (ER) or OR. There was reasonable agreement between NICO and TDCO for NICO to be a clinically acceptable method for cardiac output measurement.38 In another study, consistent lower values were observed with NICO than TDCO.39 Therefore, it is used to monitor percentage change in stroke volume and cardiac index following fluid bolus. In our experience, we have found it to be useful to guide fluid therapy in elderly trauma patients. However, in presence of lung pathology, it becomes less reliable. Ultrasound for Hemodynamic Monitoring in Trauma Ultrasound modalities that allow measurements of dynamic parameters to determine preload dependency of the patient include transthoracic echocardiography (TTE), transesophageal echocardiography (TEE), esophageal Doppler and ultrasound of the inferior vena cava (IVC). As compared to the conventional imaging, which requires significant training and skills for sonography, abridged focussed studies can be done in trauma patients to identify specific trauma related problems with little training.40 Various information that can be obtained from these methods are: 1. Recognition of hematomas and free blood in abdomen 2. Recognition of pericardial effusion and tamponade 3. Estimation of fluid responsiveness by IVC diameter changes during respiration 4. Estimation of preload using right and left ventricular end diastolic volumes


Essentials of Trauma Anesthesia and Intensive Care

5. Assessment of ventricular function via fractional area change


6. Detection of regional wall motion abnormalities 7. Assessment of valvular function Focussed Assessment Sonography in Trauma (FAST) Some trauma injuries may not be apparent at the initial physical examination. Patients can present with distracting injuries or altered mental status. Significant occult bleeding into the peritoneal, pleural, or pericardial spaces may occur without obvious warning signs. This free fluid (usually blood) can be rapidly identified by bedside ultrasound in trauma. Advanced Trauma Life Support (ATLS®) protocol also supports use of FAST in ER in hemodynamically unstable patients.1 As this is a rapid, non-invasive diagnostic test, it can be performed by a trauma surgeon/ER physician or by a radiologist while other resuscitative procedures are going on. The probe locations for FAST views are right upper quadrant, left upper quadrant, pericardial space and pelvis (Fig. 9.3). The normal ultrasound views and the scans showing free fluid collection at various sites have been shown in Figures 9.4–9.7. Based upon FAST diagnosis, possibility of hemodynamic changes can be expected and decision of exploratory laparotomy can be taken before clinical deterioration occurs.

(b) Pericardium



Fig. 9.4: Four chamber view of normal heart and liver as seen in the subxiphoid view (a). Free fluid seen in pericardial space (b) (RA-right atrium, LA-left atrium, RV-right ventricle, LV-left ventricle and IAS-interatrial septum)

Transthoracic Echocardiography (TTE)

Fig. 9.3: Site of probe placement for focussed assessment sonography in trauma (FAST) examination. The probe locations for FAST views are right upper quadrant, left upper quadrant, pericardial space and pelvis

TTE is a useful tool to assess cardiac function as well as fluid volume status besides identification of cardiac trauma and pericardial tamponade and can be performed noninvasively and rapidly by ER physician.41 As compared to the standard detailed echocardiography, various modifications have been used for rapid assessment in trauma patient, suitable for an emergency physician to perform.

Hemodynamic Monitoring in a Trauma Patient 141 (a)

(b) Superior (Chest)

Inferior (Abdomen)

Free fluid (Blood) in Morison’s pouch

Liver Diaphragm Liver

Right kidney

Right kidney Right lung

Fig. (b) 9.5: Normal right upper quadrant view showing liver, diaphragm and Morison’s pouch (a) Free fluid seen in Morison’s pouch (b) (a)

(b) Superior (Chest)

Inferior (Abdomen)

Superior (Chest)

Inferior (Abdomen) Free fluid (Blood)

Diaphragm Spleen

Left kidney Left lung

Spleen Left kidney

Fig. 9.6: Normal left upper quadrant view showing spleen, diaphragm and kidney (a). Free fluid seen in between spleen and kidney (b)

The bedside echocardiographic assessment in trauma/ critical care (the BEAT examination) involves use of a portable ultrasonography device to obtain four cardiac views— parasternal long axis, parasternal short axis, apical 4 chamber and subxiphoid views.42 It provides information about—B: Beat/cardiac index, E: Effusion, A: Area/ventricular size and function and T: Tank/preload. Focussed rapid echocardiographic evaluation (FREE) is similar but little complex comprehensive TTE examination which also measures left ventricular ejection fraction, stroke volume, cardiac output and cardiac index.43 An excellent agreement was seen when these non-invasive methods were

compared with PAC based cardiac output techniques, but less with arterial line based techniques (Flo-TracVigilio) especially in patients with ejection fraction less than 40%.43 Such limited transthoracic echocardiogram (LTTE) has been found to be a useful tool to guide fluid therapy in hypotensive trauma patients.44 Transesophageal Echocardiography (TEE) TEE is a semi-invasive procedure that should be performed by a trained physician who understands its indications and potential complications. In patients with trauma, the TEE is an excellent monitor of ventricular performance, blood


Essentials of Trauma Anesthesia and Intensive Care



Short axis




Free fluid

Fig. 9.7: Suprabubic (short axis) view showing normal scan in a male patient (a). Free fluid seen around urinary bladder in a male patient (b)

volume and adequacy of fluid resuscitation. The TEE allows imaging of the left ventricular outflow tract in real-time. The assessment of preload is based on visual inspection of end diastolic area and end systolic area of left ventricle. One must consider other confounding factors as right ventricular failure, vasodilatation and use of inotropic agents.45 Right ventricular end diastolic volume index (RVEDVI) measurement may be considered as a better indicator of adequacy of volume resuscitation than CVP or PCWP46 and avoids morbidity associated with the invasive method.15 Many patients with ‘acceptable’ PAOP parameters may in fact have inadequate left ventricular filling.47 Assessment by TEE has altered resuscitation management in such patients. Results of TEE are not affected by artifact introduced by positive pressure ventilation. 15 Other advantages of TEE in trauma include assessment of ventricular function, wall motion abnormalities, valvular disease, pericardial effusion, cardiac tamponade, aortic injury, interatrial shunt and pulmonary embolism. TEE has been found to be equal to computed tomogram in diagnosing aortic and cardiac trauma.48

of injury, withdrawal of the naso- or orogastric tube has been recommended prior to TEE insertion.

Apart from these benefits in ER or ICU setups, so far there are no clear cut recommendations of intraoperative use of TEE as an effective monitoring tool in trauma patients. In elderly trauma patients, perioperative use of TEE may be beneficial as it provides information about cardiac wall motion and structural abnormalities. Because of the possibility of exacerbating an esophageal rupture, patients with known or suspected esophageal injury should not have a TEE placed. In all other patients, in order to reduce risk

IVC assessment requires only basic level training, enables quick evaluation, and can be easily integrated into routine procedures, like FAST.11 The IVC is a highly compliant vessel with no valves and can be easily distended. The IVC is identified with two-dimensional (2-D) imaging as an extension of cardiac TTE or FAST. In presence of hypovolemia, IVC diameter reduces significantly during inspiration. More than 50% reduction in diameter is usually associated with CVP 3 cm are unlikely to respond to fluid volume, and with IVC diameter 6 mmol/L is a marker of severe injury in all patients.56 In another study, a base deficit of >8 mmol/ L predicted a 25% mortality rate in trauma patients.57 Preexisting diseases, like diabetic ketoacidosis and renal failure, can alter base deficit levels. Initial base deficit, however, is a poor predictor of mortality.58 Serum Lactate Lactic acid is a byproduct of anaerobic metabolism after glycolysis and is a circulating biomarker of tissue oxygen debt. Serum lactate is a sensitive early marker of degree of tissue hypoperfusion. As lactic acid is removed from the body more slowly than blood gases, it gives more approximation with severity of shock.59 Though serum lactate level above 2 mmol/L is considered elevated,60 in critically ill patients, often higher levels are seen.61 Trends in serum lactate levels can also be used to monitor the resuscitation even in those patients who do not show any signs of physiologic perturbation. The resuscitative

measures that decrease lactate values within 24 hours to normal are considered effective resuscitation. Serial lactate levels can also be used to predict a bad prognosis in trauma patients.60 Persistently, elevated lactate levels are significantly correlated with higher mortality and considered to be superior to base deficit levels.58 It was found that both base deficit and lactate levels correlated with transfusion requirements, whereas mixed venous O2 saturation did not. Therefore, patients with higher base deficit and lactate levels are at the greatest risk of developing hemodynamic instability and need for blood transfusion.62 Base deficit is also predictive of higher mortality and development of organ failures, like acute respiratory distress syndrome (ARDS).63 In a meta-analysis, it was observed that use of serum lactate estimation in critically ill patients has the potential to alter therapeutic decisions as hyperlactatemia in critically ill patients is often interpreted as a result of systemic oxygen imbalance, triggering goal-directed therapy. However, there is still insufficient data to prove that such therapy improves outcome in trauma patients.64 Mixed Venous or Central Venous Oxygen Saturation Pulmonary artery blood sampling allows measurement of true mixed venous oxygen saturation (SvO2) reflecting overall oxygen extraction whereas sample from a central venous catheter usually measures oxygen saturation (ScvO2) in the superior vena cava which principally reflects the degree of oxygen extraction from the brain and the upper part of the body.65 Continuous SvO2 is measured from pulmonary artery using Swan-Ganz Oximetry TD system involving reflection spectrophotometry.66 It has been shown to correlate closely with tissue perfusion and responds rapidly to changing clinical conditions. It is mostly used in ICU setup where PAC is in place. In normal patients, both SvO2 and ScvO2 are closely related and SvO2 can be calculated from ScvO2.67 Though considered as a surrogate marker of SvO2, ScvO2 may differ significantly in shock states.68 Normal SvO2 values are 65–75%.68 A decreased SvO2 or ScvO2 value is a marker of inadequate global oxygenation, if cardiac output decreases, tissue perfusion decreases (hypovolemia, shock) or if oxygen extraction of tissues increases (fever, seizures, stress). Increased ScvO2 in a trauma patient, on the other hand may reflect either an increase in O2 delivery relative to O2 consumption, in an adequately resuscitated and stabilized patient, or a reduction

Hemodynamic Monitoring in a Trauma Patient 145

in O2 consumption relative to O2 supply.27 Hence, a normal ScvO2 should not be interpreted alone as both low perfusion and low oxygen consumption may be simultaneously present. Once ScvO2 has been restored to >70%, other measures to assess microcirculation, like serum lactate, should be used to judge tissue perfusion. 69 In trauma patients with hemorrhage, additional resuscitation or surgery is required when SvO2 has been found to be 500 mL/min/m2 was indistinguishable from DO2I >600 mL/min/m2 and this goal is easier to achieve with volume loading.76 It is actually associated with decreased intestinal perfusion and increased incidence of abdominal compartment syndrome.77 Its true value in monitoring the resuscitation is yet to be confirmed. Tissue Oximetry Tissue oxygenation in critical trauma patients may be impaired secondary to regional vasoconstriction. These compensatory stress states can be detected by tissue oxygen saturation (StO2). Non-invasive measurement of StO2 using near infrared spectroscopy (NIRS) is a valid method to monitor regional tissue oxygen delivery, especially in septic and trauma patients.78 It is sensitive to both arterial oxygen content and skin perfusion, and it will reflect decreases in any of these much before pulse oximetry shows any decrease in saturation.

Oxygen uptake is the amount of oxygen taken up by the tissues. It can be estimated by calculating mixed venous oxygen content and finding the difference between oxygen delivery and the oxygen in the mixed venous blood. The oxygen content of mixed venous blood is normally about 15 mL/100 mL. Normally, the ratio of VO2 to DO2 (extraction ratio) is about 20–30%74 but if tissue demand increases, it can double.

NIRS based oximetry is conventionally used to monitor cerebral oximetry to diagnose cerebral ischemia during cardiac surgery or in severe head trauma patients. Though reliable, NIRS alone is not complete and accurate enough to monitor the brain oxygenation.79 Recently, it is also used as somatic oximetry to monitor tissue oxygenation in acute trauma patients.80 It involves measuring near-infrared tissue oximetry of vulnerable muscle beds, usually on the thenar eminence. This technique is easy to use and gives musclebed tissue saturation that correlates closely with other indices of tissue oxygenation.81,82 NIRS can be used to identify regional tissue hypoperfusion and guide therapy. In a recent study, NIRS-derived StO2 obtained on arrival of patient predicted the need for blood transfusion in patients who initially seem to be hemodynamically stable (systolic blood pressure >90 mm Hg).83 A minimum StO2 less than 70% correlated with the need for blood transfusion with a sensitivity of 88% and a specificity of 78%.84 It has also been used to predict multisystem organ dysfunction and death in severe trauma85 and to monitor free flaps after microvascular surgeries.86 However, in another study, significant reductions in StO2 were noted only in severe shock with marginal reductions in mild to moderate shock.87

Though it was proposed that in shock resuscitation, a supranormal oxygen delivery index DO2I >600 mL/min/m2 should be maintained to improve outcome, this has been

Induction of anesthesia can alter the StO2 due to vasodilatation but its exact effects on StO2 are yet to be studied.88

Oxygen Delivery and Oxygen Uptake The primary goal of the cardiorespiratory system is to deliver adequate oxygen to satisfy tissue metabolic requirement and maintain balance between oxygen delivery (DO2) and oxygen uptake (VO2). The delivery of oxygen is calculated by multiplying the arterial oxygen content (CaO2) by the cardiac output (CO). The oxygen content of arterial blood is calculated using hemoglobin concentration, oxygen saturation and PaO2 using the equation: CaO2= (O2 carried by Hb) + (O2 in solution) = (SaO2 × Hb × 1.34) + (0.003 × PaO2) × Hb × SpO2 × 0.01) + (0.003 × PaO2)


Essentials of Trauma Anesthesia and Intensive Care

Gastric Tonometry

P(v-a)CO2= VCO2/(Cardiac output × k)

Gastric tonometry is a method of organ-specific monitoring of the status of the splanchnic circulation. On the regional level, compensated shock decreases blood flow to the splanchnic bed to a larger extent while maintaining cerebral and coronary blood flow.53 The blood flow distribution away from the gastrointestinal tract, results in an increased anaerobic metabolism and increased gastric mucosal CO2 leading to gastric mucosal acidosis. The intramucosal pH (pHi) and the difference between intragastric PCO2 and arterial PCO2 (PCO2 gap) is correlated well with degree of gastric hypoperfusion.46 As compared to the original balloon tipped intragastric catheter device, recently developed fiberoptic systems using a spectrophotometric continuous monitoring are less cumbersome.

Venoarterial gradient is proportional to production of CO2 (VCO2) and inversely proportional to cardiac output.27 As CO2 washout is dependent upon tissue perfusion, local or regional low flow will increase tissue CO2 collection at tissue levels, leading to increased diffusion of CO2 from hypoperfused tissue to venous blood, leading to an increase in venoarterial gradient for CO2. A P(v-a) CO2 >6 mm Hg is indicative of inadequate tissue perfusion.98 In head injured patients, however, elevated cerebral venous to arterial gradient of CO2 when collected from jugular bulb was associated with better neurological outcome when oxygenation is unaffected.99

A positive correlation is found between pHi 10 units RBCs in 24 hours; loss of half of blood volume within 3 hours; use of 50 units of blood components in 24 hours; or use of 6 units RBCs in 12 hours.5 In children, it is defined as transfusion of more than 40 mL/kg.6 A dynamic and practical definition is the requirement of more than four RBC units within an hour7 or blood loss more than 150 mL/ min with hemodynamic instability and need for transfusion.5 Regardless of the definition used, each of these definitions aim at ensuring early identification of patients with lifethreatening bleeding, proper resuscitation and prevention of complications associated with resuscitation.8 TRADITIONAL APPROACH TO HEMORRHAGE AND CONSEQUENCES OF AGGRESSIVE VOLUME RESUSCITATION Historically, resuscitation has been initiated with a large volume of crystalloid/colloid and PRBCs followed by

Massive Blood Transfusion

supplementation with plasma, platelets and cryoprecipitate on the basis of laboratory test values and at the discretion of the anesthetic and surgical teams.9 Aggressive fluid resuscitation is complicated by pulmonary edema, exacerbation of thrombocytopenia and coagulopathy due to hemodilution. Furthermore, the pro-inflammatory nature of crystalloids10 with increased risk of infection has been recognized. 11,12 Red cell concentrates do not contain coagulation factors or platelets whereas, all blood components may be necessary in patients with massive hemorrhage (MH). Recent literature supports the use of smaller amounts of crystalloids and larger amounts of FFP in the initial resuscitation period as it is associated with improved 24-hour and 30-day survival.13,14 Some studies recommend that plasma and platelet transfusion be withheld until the prothrombin time (PT) or activated partial thromboplastin time (aPTT) is 1.5 times normal. 4,15 However, there is a significant time interval between the ordering of tests and availability of results. Therefore, laboratory-guided component therapy is limited as a guiding tool during massive bleeding.16 Rapid treatment of initial coagulation disturbances improves survival.17,18 Clinical studies emphasize the importance of identification and aggressive treatment of coagulopathy in the early stages of presentation.19 Transfusion of blood and blood products in a standardized and protocolized method has been advocated to achieve this. MASSIVE TRANSFUSION PROTOCOL (MTP) An MTP is a standardized method of treating patients identified to be at high risk for requiring an MT. MTPs provide an algorithmic, proactive, ratio-based approach to facilitate timely blood product release and mitigate blood bank delays.20,21 Without predefined guidelines, availability of appropriate volume and ratio of blood products to the patient may be significantly delayed. Causes of potential delay include physical ordering of the blood, communication, and decision-making between involved parties, sending of laboratory samples and timely receipt of their results.22 Development of an institution-based standardized protocol for MT should include specialists from the emergency medicine, trauma surgery, critical care, anesthesia, transfusion medicine, hematology and nursing departments.22 At present, there are no ‘best practice’ guidelines for the management of uncontrollable hemorrhage and coagulopathy because of limited evidence. Each trauma center has


developed its own MTP and the optimal clinical management is still under debate. Goals of MTP The purpose of MTP is (a) To provide blood products to hemodynamically unstable trauma patients in an immediate, sustained, uniform and predefined manner.22 (b) To prevent and control coagulopathy and decrease further hemorrhage after trauma.5 The overall goal is to improve patient outcome in MT. Models of MTP There are three basic MTP models for blood product administration, which can be used singly or in combination. These include laboratory test result-based blood product administration (component approach), predetermined blood product administration, and real-time transfusion service physician involvement to oversee blood product administration.23 Each institution should develop its MTP, based on its specific patient needs and available resources. Laboratory Test Result-Based Blood Product Administration or Component Therapy-Based Approach In the recent past, resuscitation and transfusion protocols started with administration of significant crystalloid and/or colloid, and PRBCs. This was followed by component therapy based on clinical findings and laboratory results to guide blood product choices, volumes and timing.23 An example of using component therapy is to base transfusion on hemoglobin 1.5 times normal, platelet count 1:1.5. Shaz et al.34 found that high as compared to low transfusion ratios of FFP, platelets, and cryoprecipitate to PRBCs were associated with improved 30-day survival.

Massive Blood Transfusion

In contrast, some studies refute these findings. 48,49 Gunter et al. reported that mortality was not reduced in patients receiving ratios of 1:1 compared to those receiving a 2:3 ratio.50 Similar results were reported by Kashuk et al.,49 however, their findings may represent a type II error. 22 The updated European guidelines for the management of bleeding following major trauma have recommended early treatment with plasma at a dose of 10 to 15 mL/kg and do not recommend a specific plasma: RBC ratio due to lack of well-designed studies and randomized controlled trials (RCTs) on this subject.24 Fixed ratio transfusion with a ratio of 1:1:1 for RBC: FFP: platelets seems the most promising, considering the current data.9,13,31,39,44,51 The optimal FFP:RBC and the platelets: RBC ratios remain to be established. Despite the lack of consensus, it is evident that the practice of fixed ratio transfusions in the form of a consistent protocol has led to a significant reduction in mortality from more than 90% to between 30 and 70%. 52 Advantages of predetermined ratios include early aggressive blood product support, decreased overall blood product usage, improved patient outcome, standardization and decreased errors. Limitations of Current Data on Predetermined Blood Product Administration: Majority of the studies on predetermined blood product administration are retrospective, confounded by unmeasur-able variables and subject to bias (survivor and selection bias) and hence should be interpreted with caution. Survivor bias means that plasma and platelets were available only for those patients who were bleeding slowly enough to receive them and that rapidly bleeding patients died before receiving blood products. Selection bias means that more resources, including plasma and/or platelet transfusions, may have been expended on the patients deemed most likely to survive.53 In addition, most of the studies that recommend 1:1:1 ratio of components do not achieve this ratio.6 Real-Time Transfusion Service Physician Involvement In this approach, the transfusion service physician is notified when a patient has been massively transfused or MT is anticipated. The transfusion service physician may guide the trauma team with regard to blood product administration, take primary responsibility for monitoring the patient’s coagulation laboratory values54 and can participate in inventory management to help ensure that adequate amount of blood products are available and delivered to the patient.23


COMPONENTS OF MTP The components of MTP include predicting the need for activation of MTP while following the general principles of management of acutely bleeding patient, activating the MTP with multidisciplinary communication and implementing hemostatic resuscitation with transfusion of blood and blood products in fixed ratio. Surgical hemostasis or radiologic aided embolization to arrest bleeding, cell salvage, measures to prevent lethal triad and administration of antifibrinolytics and recombinant activated factor VII (rFVIIa) are also important aspects and complementary to MTP. Once the end points of resuscitation have been achieved, deactivating MTP to avoid wastage should also be followed. The components of MTP have been summarized in Table 10.1. General Principles of Management of Acute Hemorrhagic Shock The massively bleeding trauma patient requires concurrent hemorrhage control and blood replacement therapy. Advanced Trauma Life Support (ATLS) ® guidelines recommend ABC approach in managing hemorrhagic shock in which airway and breathing receive priority over circulation (bleeding).55 The management of airway and breathing problems may improve the ‘shock state’ by improving oxygenation. High FiO 2 is administered. Intravenous (IV) access is secured; an 18, 16 or 14-gauge peripheral IV line or an 8-Fr central access is ideal in adults. In the event of failure, intraosseous or surgical venous access may be required.30 At the start of resuscitation, blood should be taken for group and cross-match, coagulation tests, full blood count and biochemistry. Patients with uncontrollable hemorrhage and coagulopathy (abdominal, vascular, thoracic, pelvic trauma) are identified. Predicting the Need for MTP Activation Several scores have been developed to guide MTP activation. It is imperative that the scoring systems be used to augment, and not replace, clinical decision making. The ‘Assessment of Blood Consumption’(ABC) score uses arrival tachycardia (heart rate >120 bpm), hypotension (systolic blood pressure i.e. SBP 8 g/dL Maintain platelet count >75 × 109; anticipate platelet count 100 × 109/L if, multiple or CNS trauma or if platelet function is abnormal Maintain prothrombin time and APTT 1.13 mmol/L Maintain fibrinogen >1.0 g/L; if not corrected by FFP, give cryoprecipitate (two packs of pooled cryoprecipitate for an adult) Fully compatible blood–time permitting Hypotensive resuscitation: Maintain systolic blood pressure 80–100 mm Hg until hemorrhage is controlled is recommended, unless there is concern for traumatic brain injury Prevent and treat “lethal triad”, i.e. hypothermia, acidosis and coagulopathy Actively warm the patient and all transfused fluids Ensure conventional measures to prevent and treat coagulation Correct coagulopathy by the judicious use of blood component therapy Monitoring: Base deficit and lactate levels (adequacy of resuscitation in restoring oxygen delivery and tissue perfusion) Electrolytes Correction of electrolyte abnormalities: Hyperkalemia (large volume of banked RBCs) Hypocalcemia (citrated anticoagulants) Sodium and chloride abnormalities (crystalloid resuscitation) Consider damage control surgical management strategies Consider administration of antifibrinolytic agent: Tranexamic acid within 3 hours of massive hemorrhage Consider the administration of recombinant activated factor VIIa (rFVIIa) only in clinically appropriate circumstances When appropriate, warfarin reversal with prothrombin complex concentrate; heparin reversal with protamine Continue follow-up care Deactivating the MTP: The team leader should inform the blood bank when MTP is over, to avoid wastage Documentation of the blood products administered Auditing: Review each MTP activation and execution: Done by a transfusion medicine service physician within 24 hours Initiate feedback from participants involved in the MTP Report oversight related to MTP (product wastage and non-compliance to infuse components in designated ratios)

Massive Blood Transfusion

The trauma-associated severe hemorrhage (TASH) score uses seven independent variables that include SBP, gender, hemoglobin, fluid on ultrasound, pulse, base excess, and extremity or pelvic fractures. 57 McLaughlin et al. 58 identified four factors that were associated with risk for MT: heart rate >105 bpm, SBP1.5–2.0 g/L and platelet count (>50,000–100,000 × 10 9 /L) are necessary for drug efficacy.5 In the CONTROL trial76 rFVIIa decreased RBC, FFP and total allogenic blood product use, but did not affect mortality. Because of controversial evidence and high cost, the routine use of rFVIIa in trauma patients is not recommended. The use of this agent in trauma patients at many institutions remains restricted and is not incorporated into their MT protocols.35,77

Massive Blood Transfusion


Fig. 10.1: The “lethal triad” of major trauma5

Approval to use rFVIIa is required from at least two consultants who evaluate the patient who is likely to die due to ongoing bleeding or ongoing massive requirement of blood products.78 This should be documented in the patient’s medical record. It is administered after consultation with hematologist to confirm appropriateness of optimal conventional therapy for coagulopathy and the appropriate dosage of rFVIIa.78 The dose is 90 µg/kg, given by IV bolus over 2–5 minutes and administered within 3 hours of reconstitution.78 The dose should be rounded off to the nearest 1.2 mg vial size to avoid wastage. 78 Sodium bicarbonate should be used to temporarily correct acidosis,

if pH 50%), partial pressure of mixed venous oxygen (65 years, receiving rFVIIa (9.0%). Because of the risk of serious adverse effects, treatment with rFVIIa must be individualized based on a risk-benefit analysis.

Administration Guidelines

Preconditions for rFVIIa Administration Fibrinogen levels of >50 mg dL-1 (preferably 100 mg dL-1) and platelet levels of >50 × 109 L-1 and 100 × 109 L-1 in case of head trauma are the preconditions for rFVIIa administration. If these parameters cannot be monitored in ‘real-time’ by point of care testing, the patient should receive appropriate empirical replacement therapy. Correction of the pH to >7.2 is recommended prior to its administration. rFVIIa and Surgical Hemostasis 1. rFVIIa should be administered as an adjunctive therapy to concomitant surgical measures, as the agent arrests coagulopathic, rather than surgical bleeding. 2. If packing was performed, unpacking should be considered before administration of rFVIIa. 3. If hemorrhage is encountered outside the operating room, angiography or a ‘second look’ should be

182 Essentials of Trauma Anesthesia and Intensive Care

considered (depending on the clinical circumstances) to rule out surgical bleeding. Dosage The recommended initial dose of rFVIIa for treatment of massive bleeding is 120 (100–140) g kg-1 administered intravenously over 2–5 min. Repeat Dosage If hemorrhage persists beyond 15–20 min, following the first administration of rFVIIa, an additional dose of 100 g kg-1 should be considered. If the response remains inadequate following a total dose of >200 g kg-1, the preconditions for rFVIIa administration should be re-checked, if possible, and corrected as necessary before a third dose is considered. If this is not feasible, the empirical administration of FFP (10–15 mL kg-1 or 4–6 U for 70 kg), cryoprecipitate (1–2 U 10 kg-1 or 10–15 U for 70 kg), and platelets (1–2 U 10 kg-1 or 10–15 U for 70 kg) should be considered, and the pH and calcium should be checked and corrected. Only after these measures have been applied should a third dose of rFVIIa 100 g kg-1 be administered.

hospitals in 40 countries and 20,211 adult trauma patients with or at risk of significant bleeding were randomly assigned within 8 hours of injury to either tranexamic acid (loading dose 1 g over 10 min then infusion of 1 g over 8 hours) or matching placebo.96 All cause mortality was significantly reduced with tranexamic acid (14.5%) vs placebo group (16.0%). The analysis of the 2010 CRASH-2 study published in The Lancet in 2011 shows that tranexamic acid should be given as early as possible to bleeding trauma patients; if treatment is not given until three hours or later after injury, it is less effective and could even be harmful.97 The Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) study evaluated outcomes in 896 patients who were treated with tranexamic acid or not.98 Unadjusted mortality rates were significantly reduced for treated (17 versus 24%) versus non-treated casualties. In patients requiring massive transfusion, greater reductions in mortality were seen for those who were treated with tranexamic acid (28 versus 14%). Other antifibrinolytic agents include aminocaproic acid and aprotinin, but these have not been evaluated in patients with traumatic coagulopathy.99 Sex Hormones

Monitoring Currently, there is no laboratory method for monitoring the effect of rFVIIa. The best available indicator of rFVIIa efficacy is the arrest of hemorrhage judged by visual evidence, hemodynamic stabilization and a reduced demand for blood components. The PT is expected to shorten, frequently below the normal expected range, but this does not reflect efficacy. ROTEM® and thrombin generation are future candidate tests for evaluation of efficacy of rFVIIa. As a result of the lack of controlled trials, these guidelines should be considered as suggestive rather than conclusive. However, they provide a valuable tool for physicians using rFVIIa for the expanding off-label clinical uses. Antifibrinolytic Agents Antifibrinolytic therapy may be appropriate in patients with ongoing hemorrhage with depleted fibrinogen. Tranexamic acid blocks the lysine binding site of the plasmin molecule irreversibly, thereby blocking the binding of plasminogen to tissue plasminogen activator and to fibrinogen, which is needed for activation.24 Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage (CRASH-2) trial was undertaken in 274

Experimental studies in animals show that female rats are more resistant to acute trauma-hemorrhagic shock-induced gut and lung injury than male rats.100 The protection is related to the hormonal status of the rat at the time of injury with maximal protection during the proestrus and estrus stages of the cycle when estrogen levels are highest. Several epidemiologic studies report low incidence of post-traumatic infection and multi-organ failure and increased survival in younger (premenopausal) women with severe injuries.101-104 Sex hormones are believed to modulate the immune response to shock and sepsis in improving the survival.105 Thus, alteration or modulation of the hormonal levels at the time of injury could be a novel therapeutic option for improving the outcome. However, it needs additional clarification from future experimental studies and clinical trials. SUMMARY Trauma patients with an established coagulopathy have high mortality, and must be diagnosed as early as possible and managed aggressively. The increasing use of point-of-care monitoring with TEG® and ROTEM® helps in the rational use of blood products, such as fresh frozen plasma, platelet, fibrinogen and prothrombin complex concentrate.

Coagulopathy in Trauma: Pathophysiology and Management

Tranexamic acid should be given as early as possible to bleeding trauma patients; if treatment is not given until three hours or later after injury, it is less effective and could even be harmful. Use of recombinant factor VIIa has shown to decrease bleeding but its effects on better outcome need to be proven in a well-controlled clinical trial. Sex hormones are believed to modulate the immune response to shock and sepsis in improving the survival and could be a novel therapeutic option for improving the outcome. However, it needs additional clarification from future experimental studies and clinical trials.


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Theusinger OM, Wanner GA, Emmert MY, et al. Hyperfibrinolysis diagnosed by rotational thromboelastometry (ROTEM) is associated with higher mortality in patients with severe trauma. Anesth Analg 2011;113:1003–12.


Tauber H, Innerhofer P, Breitkopf R, et al. Prevalence and impact of abnormal ROTEM® assays in severe blunt trauma: Results of the ‘Diagnosis and Treatment of Trauma-Induced Coagu lopathy (DIA-TRE-TIC) Study’. Br J Anaesth 2011;107:378–87.


Spahn DR, et al. Management of bleeding following major trauma: A European guideline. Available online at: http://


De Biasi AR, Stansbury LG, Dutton RP, et al. Blood product use in trauma resuscitation: Plasma deficit versus plasma ratio as predictors of mortality in trauma (CME). Transfusion 2011;51:1925–32.


Brown LM, Aro SO, Cohen MJ, et al. A high fresh frozen plasma: Packed red blood cell transfusion ratio decreases mortality in all massively transfused trauma patients regardless of admission international normalized ratio. J Trauma 2011; 71:S358–63.


Gonzales EA, Moore FA, Holcomb JB, Miller CC, Kozar RA, Todd SR, et al. Fresh frozen plasma should be given earlier to patients requiring massive transfusion. J Trauma 2007;62: 112–19.


Dara SI, Rana R, Afessa B, Moore SB, Gajic O. Fresh frozen plasma transfusion in critically ill medical patients with coagulopathy. Crit Care Med 2005;33:2667–71.


Khan H, Belsher J, Yilmaz M, Afessa B, Winters JL, Moore SB et al. Fresh-frozen plasma and platelet transfusions are associated with development of acute lung injury in critically ill medical patients. Chest 2007;131:1308–14.


Sarani B, Dunkman WJ, Dean L, Sonnad S, Rohrbach JI, Gracias VH. Transfusion of fresh frozen plasma in critically ill surgical patients is associated with an increased risk of infection. Crit Care Med 2008;36:1114–18.


Nienaber U, Innerhofer P, Westermann I, Schochl H, Attal R, Breitkopf R, et al. The impact of fresh frozen plasma vs coagulation factor concentrates on morbidity and mortality in trauma-associated haemorrhage and massive transfusion. Injury 2011;42:697–701.


Watson GA, Sperry JL, Rosengart MR, Minei JP, Harbrecht BG, Moore EE et al. Fresh frozen plasma is independently associated with a higher risk of multiple organ failure and acute respiratory distress syndrome. J Trauma 2009;67:221–27.


Kashuk JL, Moore EE, Johnson JL, et al. Postinjury lifethreatening coagulopathy: Is 1:1 fresh frozen plasma: Packed red blood cells the answer? J Trauma 2008;65:261–70.


Sperry JL, Ochoa JB, Gunn SR, et al. An FFP: PRBC transfusion ratio >/=1:1.5 is associated with a lower risk of mortality after massive transfusion. J Trauma 2008;65: 986–93.



Scalea TM, Bochicchio KM, Lumpkins K, et al. Early aggressive use of fresh frozen plasma does not improve outcome in critically injured trauma patients. Ann Surg 2008;248:578–84.


Kheirabadi BS, Crissey JM, Deguzman R, Holcomb JB. In vivo bleeding time and in vitro TEG measurements are better indicators of dilutional hypothermic coagulopathy than prothrombin time. J Trauma 2007;62:1352.


Martini WZ, Cortez DS, Dubick MA, et al. Thromboelastography is better than PT, aPTT and activated clotting time in detecting clinically relevant clotting abnormalities after hypothermia, hemorrhagic shock and resuscitation in pigs. J Trauma 2008;65:535.


Schöchl H, Nienaber U, Hofer G, et al. Goal-directed coagulation management of major trauma patients using thromboelastometry (ROTEM)-guided administration of fibrinogen concentrate and prothrombin complex concentrate. Crit Care 2010;14:R55.


Royston D, von Kier S. Reduced hemostatic factor transfusion using heparinase-modified thromboelastography during cardiopulmonary bypass. Br J Anesth 2001;86:575–78.


Stahel PF, Moore EE, Schreier SL, et al. Transfusion strategies in post-injury coagulopathy. Curr Opin Anesthesiol 2009; 22:289.


Fenger-Eriksen C, Jensen TM, Kristensen BS, Jensen KM, Tonnesen E, Ingerslev J, et al. Fibrinogen substitution improves whole blood clot firmness after dilution with hydroxyethyl starch in bleeding patients undergoing radical cystectomy: A randomized, placebo-controlled clinical trial. J Thromb Haemost 2009;7:795–802.


Karlsson M, Ternstrom L, Hyllner M, Baghaei F, Flinck A, Skrtic S, et al. Prophylactic fibrinogen infusion reduces bleeding after coronary artery bypass surgery. A prospective randomised pilot study. Thromb Haemost 2009;102:137–44.


Rahe-Meyer N, Pichlmaier M, Haverich A, Solomon C, Winterhalter M, Piepenbrock S, et al. Bleeding management with fibrinogen concentrate targeting a high-normal plasma fibrinogen level: A pilot study. Br J Anaesth 2009;102: 785–92.


Rahe-Meyer N, Solomon C, Winterhalter M, Piepenbrock S, Tanaka K, Haverich A, et al. Thromboelastometry-guided administration of fibrinogen concentrate for the treatment of excessive intraoperative bleeding in thoracoabdominal aortic aneurysm surgery. J Thorac Cardiovasc Surg 2009;138:694– 702.


Ansell J, Hirsh J, Poller L, et al. The pharmacology and management of the vitamin K antagonists: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:204s–33s.


Hiippala ST, Myllyla GJ, Vahtera EM. Hemostatic factors and replacement of major blood loss with plasma-poor red cell concentrates. Anesth Analg 1995;81:360–65.


Dickneite G, Dörr B, Kaspereit F, Tanaka KA. Prothrombin complex concentrate versus recombinant factor VIIa for reversal of hemodilutional coagulopathy in a porcine trauma model. J Trauma 2010;68:1151–57.

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Limentani SA, Roth DA, Furie BC, Furie B. Recombinant blood clotting proteins for hemophilia therapy. Semin Thromb Hemost 1993;19:62–72.


Boffard KD, Riou B, Warren B, Choong PI, Rizoli S, Rossaint R, et. al. Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: Two parallel randomized, placebo-controlled, double blind clinical trials. J Trauma 2005;59:8–15.



Stanworth SJ, Birchall J, Doree CJ, Hyde C. Recombinant factor VIIa for the prevention and treatment of bleeding in patients without haemophilia. Cochrane Database Syst Rev 2007;18:CD005011. Hauser CJ, Boffard K, Dutton R, et al. Results of the control trial: Efficacy and safety of recombinant activated Factor VII in the management of refractory traumatic hemorrhage. J Trauma 2010;69:489–500.


Russel L Gruen, Biswadev Mitra. Tranexamic acid for trauma. Lancet 2011;377:1052–54.


Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. Arch Surg 2012;147: 113–19.


Henry DA, Moxey AJ, Carless PA, et al. Anti-fibrinolytic use for minimising perioperative allogeneic blood transfusion. Cochrane Database Syst Rev 2001;(1):CD001886.

100. Ananthakrishnan P, Deitch EA. Gut origin sepsis and MODS: The role of sex hormones in modulating intestinal and distant organ injury: A review. XX vs XY 2003;1:108–17. 101. Caruso JM, Deitch EA, Xu DZ, et al. Gut injury and gutinduced lung injury after trauma-hemorrhagic shock is gender and estrus cycle specific in the rat. J Trauma 2003;55:531–39.


Perkins JG, Schreiber MA, Wade CE, Holcomb JB. Early versus late recombinant factor VIIa in combat trauma patients requiring massive transfusion. J Trauma 2007;62:1095–99.

102. Wohltmann CD, Franklin GA, Boaz PW, et al. A multicenter evaluation of whether gender dimorphism affects survival after trauma. Am J Surg 2001;181:297–300.


Levi M, Levy JH, Andersen HF, Truloff D. Safety of recombinant activated factor VII in randomized clinical trials. N Engl J Med 2010: 363;1791–800.

103. Mostafa G, Huynh T, Sing RF, et al. Gender-related outcomes in trauma. J Trauma 2002;53:430–35.


Martinowitz U, Michaelson M, Israeli Multidisciplinary rFVIIa Task Force. J Thromb Haemost 2005;3:640.


Shakur H, Roberts I, Bautista R, Caballero J, Coats T, Dewan Y, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): A randomised, placebo-controlled trial. Lancet 2010;376:23–32.

104. George RL, McGwin G, Windham ST, et al. Age-related gender differential in outcome after blunt or penetrating trauma. Shock 2003;19:28–32. 105. Angele MK, Wichman M, Eisenmenger S, et al. Immunologic effects of sex hormones following hemorrhagic shock: Potential therapeutic applications: A review. XX vs XY 2003;1:39–45.



Intravenous Anesthetic Agents Nita D’Souza, Babita Gupta


Administration of anesthesia to trauma patients poses a unique challenge as it is often associated with blood loss and hemodynamic instability.

There is no ideal anesthetic agent and using multiple agents for their desirable effects and likewise to avoid the adverse effects are suggested.

Preferential use of induction agents with favorable pharmacological properties and conferring hemodynamic stability is essential. Rational choice needs to be made for appropriate dosing of intravenous induction agents keeping in mind the altered physiology in trauma patients.

Ketamine and etomidate are preferred induction agents in patients with hemorrhagic shock due to their hemodynamic stability.

Propofol and thiopentone should be avoided in a hemorrhagic shock patient.

INTRODUCTION A critically ill trauma patient in hemorrhagic shock presenting to emergency room (ER) or operating room (OR) often needs administration of anesthetic drugs to assist endotracheal intubation; either for protecting the airway or for providing general anesthesia prior to any surgical procedure. The choice of anesthetic agent in a trauma patient is of utmost importance, due to unique set of problems, like:

• History and detailed information may be unavailable or limited. Allergies, genetic abnormalities, and previous surgeries may pose sudden difficulties and complicate the management.

• Patients may have multiple injuries with massive blood loss, leading to hemorrhagic shock.

• Patients are often intoxicated and are to be considered as full stomach, thus requiring rapid sequence induction (RSI).

• Possibility of cervical spine injury with neurogenic shock.

• Occult injuries, such as tension pneumothorax or cardiac tamponade can manifest at unexpected times.

• Patients may have associated traumatic brain injury (TBI) or globe injury with raised intracranial pressure (ICP) or increased intraocular pressure (IOP), respectively.

• Critical to react rapidly to the changing physiology. The risks associated with intravenous anesthetic agents was first described by a surgeon, Halford in an editorial in Anesthesiology in 1943, after caring for wounded military personnel at Pearl Harbour during World War II in 1941.1 He observed increased mortality after administration of thiopentone, which was ascribed to the increased concentration of the drug action due to hypovolemia. He critiqued intravenous anesthetic agents and described them in a rather hyperbolic way as ‘an ideal form of euthanasia’! According to a survey conducted by Harrison on mortality associated with anesthesia, induction of anesthesia in a hypovolemic patient was the most common cause of death attributable to anesthesia.2 These reports highlight the fact that an appropriate anesthetic agent should be chosen for induction of anesthesia in a patient with hemorrhagic shock. Ideal choice of anesthetic agent for most trauma patients is one which facilitates safe anesthesia and brings about rapid unconsciousness without causing hemodynamic compromise and


Essentials of Trauma Anesthesia and Intensive Care

requires minimal dose reduction with high therapeutic index (safety margin). It is essential for the anesthesiologist to recognize the need to select, titrate and moderate the dosage of anesthetics prior to administration in severely hypovolemic patients. Routine dosing of certain anesthetic drugs may produce unwanted side effects causing potentially adverse consequences. It is important to understand whether blood loss and ongoing resuscitation has any bearing on the pharmacology of anesthetic drugs and it is vital to adjust the dose appropriately. Heffner remarked that most of the available clinical trials regarding the pharmacokinetics (PK) of sedative drugs have been studied for short duration and are mostly reported in normal individuals.3 Underdosing may lead to light plane of anesthesia (awareness, inadequate pain relief), having deleterious effects while overdosing possibly could cause cardiorespiratory depression in patients who are already hemodynamically compromised. Although there is literature available on PK and pharmacodynamics (PD) of anesthetic agents during hemorrhagic shock in animals; there are limited studies in humans.4-8 EFFECT OF BLOOD LOSS ON PHARMACOKINETICS AND PHARMACODYNAMICS OF INTRAVENOUS ANESTHETICS The free concentration of a drug in the target tissue, its intrinsic activity and end organ sensitivity determines the pharmacological effect of a drug. The free concentration depends upon absorption, distribution, biotransformation and excretion processes of the drug. The relationship between the dose administered and the drug concentration in different tissues is determined by these processes, i.e. PK of the drug. All these processes may be altered during hemorrhagic shock and hence change the free concentration of the drug in different tissues. Pharmacokinetics Trauma is associated with hemorrhage, leading to a reduced blood volume and cardiac output. This is accompanied by activation of sympathetic nervous system. Increased sympathetic activity causes peripheral vasoconstriction and increased cardiac contractility to maintain arterial blood pressure and cardiac output. Blood flow to the vital organs, like heart and brain, is preserved till late stages of shock despite sympathetic stimulation, whereas vasoconstriction reduces blood flowing to other organs, like skin, muscles and splanchnic organs. This disproportionate change in the

blood flow influences the PK of the drug and one or more of the four processes of drug disposition, i.e. absorption, distribution, biotransformation and excretion are affected. Absorption Since blood flow to skin, muscle and mucous membrane is decreased; oral, subcutaneous and intranasal routes are not reliable and only IV route is preferred. Distribution Intravenous induction agents in suitable dosages cause rapid loss of consciousness that starts in ‘one arm brain circulation time’ (time taken for drug to move from site of injection, i.e. arm to brain). In the event of a reduced cardiac output in shocked patients, a large proportion of the cardiac output is diverted to the cerebral circulation to preserve the cerebral blood blow (CBF). Therefore, the dose of the induction agent must be reduced as the time taken for it to reach the brain is longer in this slow circulation with prolonged effect. Homeostatic redistribution of blood flow to vital organs (brain and heart) results in higher blood concentration due to reduced blood volume and distribution. The hypovolemia in hemorrhagic shock and in critical illness alters the volume of distribution, availability and elimination of the drug thus resulting in short-acting drugs being converted into longacting drugs. Titration of the dose is essential for safe induction in hypovolemic shock patients. Similarly, the blood flow to the heart is maintained in shock and the drug concentration may be much higher in early phase, explaining the exaggerated cardiovascular response when standard doses are administered. Other factors affecting distribution are plasma protein binding and pH. In hemorrhagic shock, acute phase reactant proteins (α-1 glycoproteins) are released which bind to certain drugs and significantly reduce the free fraction of drug thus limiting its distribution. A reduction in serum albumin may contrastingly increase the free drug fraction promoting its distribution. Metabolism Majority of the drugs including anesthetic agents are metabolized in liver. Hypotension, hypothermia and sepsis are associated with hepatic dysfunction and can alter hepatic clearance of anesthetic drug. Hepatic metabolism is influenced by hepatic blood flow, free fraction of the drug and intrinsic ability of the enzymes to metabolize the drug.

Intravenous Anesthetic Agents




Excretion of the drug and its metabolites is mainly by the kidneys. Hemorrhagic shock may compromise renal perfusion resulting in decreased drug clearance. There is also an increase in tubular reabsorption as a consequence of decrease in glomerular filtration rate and urine flow.

Pharmacology of commonly available anesthetic agents in healthy individuals and trauma patients, emphasizing the impact of hemorrhage and resuscitation on their PK and PD have been described further. Propofol

Pharmacodynamics Hemorrhagic shock also has an impact on PD due to changes in the drug-receptor affinity or the alterations in the inherent receptor activity. Hemorrhagic shock may compound the effects of an intravenous anesthetic administered to a trauma patient and result even in cardiac arrest consequent to inhibition of circulating catecholamines being inhibited. Other potential factors attributing to exaggerated hemodynamic response in a hypovolemic patient include:

• Many anesthetic agents exhibit high protein binding. In severe hypovolemic shock, the non-protein bound, i.e. free drug fraction of drugs, increases resulting in an increased volume of distribution.

• Anaerobic metabolism and metabolic acidosis (respiratory or renal failure) resulting from reduced organ perfusion may modify the distribution of ionisable drugs.

• The increased potency of few anesthetic drugs (propofol) in presence of hemorrhagic shock is probably due to circulating endorphin levels which have a synergistic effect with the anesthetic agent. The commonly available intravenous induction agents are propofol, thiopentone, etomidate and ketamine. However, usage of propofol and thiopentone in trauma patients is especially problematic because both drugs are vasodilators and have a negative inotropic effect. The effect of both the anesthetics is potentiated in hemorrhagic shock. Etomidate presents as a suitable alternative in maintaining cardiovascular stability in comparison with other intravenous induction agents.9-11 Ketamine, being a sympathetic system stimulant is also popular as induction agent in trauma, though it is a direct myocardial depressant.12-14 The release of catecholamine masks cardiac depression in stable patients and on the contrary precipitates hypertension and tachycardia. Catecholamine-depleted patients may present with a cardiovascular collapse due to unmasking of the cardiac depression.15

Propofol is one of the most frequently used intravenous, induction agents in recent times. In 1977, Kay and Rolly confirmed its anesthetic property as an intravenous induction agent. Propofol (2,6-disopropylphenol), an alkyl phenol compound is an intravenous anesthetic agent, unique in having a rapid-onset and rapid-offset.16 1% propofol (10 mg/mL) is an egg lecithin emulsion formulation (diprivan), consisting of 10% soybean oil, 2.25% glycerol, and 1.2% egg phosphatide. Induction dose of propofol in healthy adults is 1.5 to 2.5 mg/kg, with blood levels of 2 to 6 µg/mL producing unconsciousness depending on the pre-medication co-administered, the patient’s physical status, age and the extent of the surgical stimulation.17 Usage of propofol with nitrous oxide for induction and maintenance of anesthesia requires an infusion rate of 120 µg/kg/min. 18 The recommended maintenance infusion rate of propofol varies between 100 and 200 µg/kg/min for hypnosis and 25–75 µg/kg/min for sedation. Awakening typically occurs at plasma propofol concentrations of 1–1.5 µg/mL.19 The induction time (onset) ranges between 22 and 125 seconds and an offset time as short as about 5 to 10 minutes is observed after a single bolus dose, as the drug rapidly redistributes after a bolus injection from central compartment [central nervous system (CNS)] into muscle, fat, and other poorly perfused tissues. Titration of doses for induction and maintenance of propofol is required in children and elderly, proportional to the central distribution volume and clearance rate. ICP, cerebral metabolic rate, and CBF appear to be decreased by the drug.20 Larger doses resulting in decreased arterial pressures can significantly decrease cerebral perfusion pressure (CPP), despite maintaining cerebrovascular autoregulation and cerebral responsiveness to carbon dioxide. Antiemetic properties of propofol are observed in the early postoperative period.21 The postulated mechanisms include depression of the chemoreceptor trigger zone, vagal nuclei, antidopaminergic activity, reduced release of glutamate and aspartate in olfactory cortex and decreased serotonin


Essentials of Trauma Anesthesia and Intensive Care

concentrations in area postrema. Propofol is a safe induction agent in patients susceptible to malignant hyperthermia unlike some inhalational and intravenous agents.

Table 12.1: Uses and doses of intravenous propofol Induction of general anesthesia

1–2.5 mg/kg IV dose reduced with increasing age and titrated in hypotensive trauma patients

Maintenance of general anesthesia

50–150 µg/kg/min IV combined with N2O or an opiate


25–75 µg/kg/min IV


10–20 mg IV, can repeat every 5–10 min or start infusion of 10 µg/kg/min

Pharmacokinetics Two-compartment kinetic model studies have shown the initial distribution half-life to be 2 to 8 minutes and the elimination half-life as 1 to 3 hours.17 Applying a threecompartment model, the initial and slow distribution halflife values are 1 to 8 minutes and 30 to 70 minutes, respectively. The elimination half-life of propofol which largely depends on the time of discontinuing the administration of propofol ranges from 2 to 24 hours. This prolonged elimination half-life is indicative of the existence of a poorly perfused compartment from which propofol slowly diffuses back into the central compartment. Propofol is rapidly cleared from the central compartment by hepatic metabolism. The context-sensitive half-life for propofol infusions of up to 8 hours is less than 40 minutes. Propofol is quickly and expansively metabolized to inactive metabolites which are removed by the kidneys. Propofol’s clearance rate (1.5 to 2.2 L/min) is more than the hepatic blood flow, signifying that an extrahepatic route of elimination (lungs) also adds to its clearance. Metabolism Glucoronide and sulphate conjugation bring about rapid metabolism of propofol to form water-soluble compounds, which are excreted by the kidneys.22 Propofol excreted in the urine is less than 1% and about 2% is eliminated in the feces.22 The metabolites of propofol are thought to be inactive. The role of the kidneys in propofol metabolism has been established, accounting for 30% of total body clearance.23,24 The lungs also may play an important role in this extrahepatic metabolism. The lungs are responsible for approximately 30% of the uptake and first-pass elimination after a bolus dose.25 Dose The uses and doses of intravenous propofol are given in Table 12.1. The recommended maximal dose of propofol infusion rate is 80 µg/kg/min (10 mmol/L-1), enlarged or fatty liver and hyperlipidemia.39 Other clinical presentations include cardiomyopathy with acute cardiac failure, hepatomegaly, lipemia, skeletal myopathy and hyperkalemia.40,41 Effect of Hemorrhagic Shock on Pharmacology of Propofol The influence of blood loss on the PK and PD of propofol has been studied by few authors. DePape et al. in his study conducted on rat models, demonstrated that moderate blood loss (17 mL/kg) results in a decrease in central compartment clearance and volume and there is also an increase in the end organ sensitivity.7 This eventually results in 2.5-fold decrease in dose to achieve same drug effect as in control group. In yet another study by Johnson et al., swine models were used to study the influence of moderate blood loss (30 mL/kg) on the PK and PD of propofol.8 Higher plasma levels of propofol and slower intercompartment clearance in the shock group was observed. There was a 2.7 times reduction in the concentration at the effect site to achieve the desired effect compared to control group. The authors also observed increased organ sensitivity to propofol by 2.5 times compared to control group suggesting that the PK changes were responsible for the changes in drug effect. Combined PK/PD model construction results indicated that the dose required to achieve a target propofol effect site concentration decreased 5.4-fold in moderate hemorrhagic shock. Effect of Hemorrhagic Shock Followed by Resuscitation on Propofol Almost all the trauma patients presenting with hemorrhagic shock would have received crystalloids. Hence, it would be


relevant to know whether volume resuscitation restores the PK and PD of anesthetic drug to baseline levels. In continuation to their previous work on swines, Johnson et al. investigated the influence of resuscitation on the pharmacology of propofol.8 Sixteen swines were randomly assigned to shock-resuscitation and control groups. The shock-resuscitation swine group were bled up to 42 mL/kg to maintain mean arterial pressure (MAP) of 40 mm Hg over 20 minutes. They were subsequently resuscitated with crystalloids to maintain MAP of 70 mm Hg over 60 minutes and were then infused with propofol. It was observed that crystalloid resuscitation restored the shock-induced changes in PK to near baseline values. However, the end organ responsiveness to propofol after hemorrhage still persisted after resuscitation although the hemodynamic parameters were near normal after resuscitation. The exaggerated hemodynamic response to propofol although reduced, but still persisted. Extrapolating these studies in clinical practice in trauma setting; it would be appropriate to reduce the dose of propofol despite resuscitation and near normal hemodynamics, to avoid undesirable cardiovascular depression and/or collapse. Rather, it would be prudent to refrain from using propofol in patients with hemorrhagic shock with/without resuscitation and if used at all, the dose should be reduced 5-fold (0.4 mg/kg). Barbiturates Barbituric acid is the condensation of malonic acid and urea. It has no central depressant activity, but the presence of alkyl/aryl groups and phenyl group at C5 confers sedativehypnotic activity and anticonvulsant activity, respectively. Oxybarbiturates and thiobarbiturates possess the C2=O and C2=S substitution, respectively. Thiobarbiturates have higher lipid solubilities. Sodium thiopental (STP) is a characteristic fast-on, fastoff barbiturate induction agent.42 STP is a sodium salt and must be dissolved in isotonic sodium chloride (0.9%) or water to prepare solutions of 2.5% thiopental. If refrigerated, solutions of the thiobarbiturates are stable for up to 2 weeks. When barbiturates are added to Ringer’s lactate or an acidic solution containing other water-soluble drugs, precipitation occurs, which can occlude the intravenous line. The redistribution half-life (t1/2) for thiopental is 5 to 8 minutes, whereas the t1/2 ranges from 5 to 17 hours. The induction dose for administration of general anesthesia in healthy, unpremedicated adult patients is between 3 and 5 mg/kg, 5 and 6 mg/kg in children and 6 and 8 mg/kg in


Essentials of Trauma Anesthesia and Intensive Care

infants. The induction time is usually within 30 to 60 seconds. The dose of barbiturates necessary to induce anesthesia is reduced in premedicated patients, patients in early pregnancy (7 to 13 weeks gestation), and those of more critical nature (American Society of Anesthesiologists grade III/IV). Geriatric patients require 30 to 40% reduction in the usual adult dose because of a reduced central compartment volume and slow redistribution of thiopental.43 Thiopental possesses a lengthy context-sensitive half-time and a similarly longer recovery time. It is metabolized in the liver to water-soluble metabolites and have little CNS activity. When high doses of thiopental are administered, a desulfuration reaction can occur with the production of pentobarbital, which has long-lasting CNS-depressant activity and low elimination clearance contributing to long elimination half-life (12 h). Elimination of phenobarbital (60 to 90%) is via kidneys unlike most barbiturates that have hepatic excretion. Metabolism Barbiturates are biotransformed by four processes: (1) oxidation; (2) N-dealkylation; (3) desulfuration; and (4) destruction of the barbituric acid ring.44 The metabolites are readily excreted in the urine or as glucuronic acid conjugates in the bile. Enzyme induction is observed with long-term administration of barbiturates.44 Thiopental is contraindicated in patients with acute intermittent porphyria because it may precipitate an attack by stimulating α-aminolevulinic acid synthetase (the enzyme responsible for the production of porphyrins).45 Barbiturates cause a centralized respiratory depression, with decreased responsiveness to hypoxia and hypercarbia. There are no significant effects on the kidneys or liver. Patients with pre-existing liver disease and hypoproteinemia tend to have a higher fraction of unbound, free (hence active) thiopental; in these patients, a reduced dose should be administered. Barbiturates cause venodilation and have negative inotropic effect. In geriatric patients, because of increased circulation time, the onset and offset of the drug tends to be delayed. Unnecessary extra dosing must be avoided in this group of patients by waiting a few seconds for the drug to achieve its effect. Titration of the dose in hemodynamically unstable patients is a must. In patients with moderately unsteady hemodynamic status, 1 mg/kg may be the appropriate dose. A dose-related depression of cerebral metabolic oxygen consumption rate (CMRO2), CBF, ICP and progressive

slowing of the electroencephalography (EEG), a reduction in the rate of adenosine triphosphate (ATP) consumption, and gaurding from incomplete cerebral ischemia is noted with barbiturates.46,47 At isoelectric EEG, when the cerebral metabolic activity is roughly 50% of baseline,48 there is no further reduction in CMRO2. They do not affect the basal metabolic function, unlike hypothermia which affects the cellular activity. Intracranial hypertension or intractable convulsions is treated with an infusion rate of 2 to 4 mg/kg/h. Thiopental is widely used to improve CPP after acute brain injury. A concurrent reduction in the ICP and MAP is observed, although the ICP decreases more relative to the decrease in MAP after barbiturate use, preserving CPP. Although barbiturate therapy is widely used to control ICP after brain injury, the results of outcome studies are no better than with other aggressive forms of cerebral antihypertensive therapy. Various theories proposed for the ‘neuroprotective properties’ are: a reverse steal (‘Robin Hood effect’) on CBF, stabilization of liposomal membranes, freeradical scavenging, as well as excitatory amino acid (EAA) receptor blockade. Barbiturates cause predictable, dosedependent EEG changes and possess potent anticonvulsant activity. Thiopental is used in status epilepticus in bolus dose of 2–4 mg/kg and further in infusion (1–5 mg/kg/hr) as drug of choice in the treatment of refractory cases.49 Patients with raised ICP, refractory to conventional treatment, respond to high dosage of barbiturates. Thiopental is used in large doses (36 mg/kg), is predisposed to cardiorespiratory depression and requires pressors and volume expansion to support cerebral perfusion. On achieving a therapeutic barbiturate effect, a maintenance dosage of 1–3 mg/kg is sufficient under continuous ECG monitoring.50 Pharmacokinetics Physiologic models of barbiturates describe a rapid mixing of the drug with the central blood volume followed by a quick distribution of the drug to highly perfused, low-volume tissues (i.e. brain) with a slower redistribution of the drug to the muscle, which terminates the effect of the induction dose. The delay of recovery when a continuous infusion of a barbiturate is used is explained by the compartmental model. This model describes: the termination of effect becomes increasingly dependent on the slower process of uptake into adipose tissue and elimination clearance through hepatic metabolism. After prolonged infusions, the pharmacokinetics of barbiturate metabolism is best approximated by non-linear Michaelis-Menten metabolism. Usual doses

Intravenous Anesthetic Agents

(4 to 5 mg/kg) of thiopental exhibits first-order kinetics (i.e. a constant fraction of drug is cleared from the body per unit time); however, at very high doses of thiopental (300 to 600 mg/kg) with receptor saturation, zero-order kinetics occur (i.e. a constant amount of drug is cleared per unit time). The volume of distribution is slightly more in female patients causing longer elimination half-lives.51,52 The clearance rate of thiopental is unaffected in cirrhotic patients because the protein availability for the drug to bind is still adequate even at advanced stages of the disease process.53 Thiopental’s fat-affinity, low rate of hepatic clearance, and relatively large volume of distribution predisposes its accumulation in the tissues, especially if administered in large doses over a prolonged period. The plasma drug level increases when repeat doses of drug are given.54 Mechanism of Action The mechanism of action of barbiturates on the CNS is primarily via the action on gamma-amino butyric acid (GABAA) receptor although recent studies have proposed the role of N-methyl-D-aspartate (NMDA) receptors.55-60 The actions of barbiturates on CNS are: 1. Enhances the synaptic actions of inhibitory neurotransmitters (GABA); and 2. Blocks the synaptic actions of excitatory neurotransmitters (glutamate and acetylcholine).61 Pharmacodynamics Barbiturates produce sedation, sleep and in sufficient doses produce a CNS depression. General anesthesia is produced which is characterized by amnesia, loss of consciousness and cardiorespiratory depression. The amnesic effect of barbiturates is less pronounced than that produced by benzodiazepines. Faster onset of action is observed in barbiturates proportionate to their high lipid solubility and low degree of ionization (most barbiturates are non-ionized) which allows their rapid access across the blood-brain barrier.56 The non-ionized form of a drug alone can directly cross the cellular membranes. Thiopental has a pKa of 7.6. Nearly 50% of thiopental is non-ionized at physiologic pH, which contributes partially to accumulation of thiopental in the cerebrospinal fluid (CSF) after IV administration.62 Larger proportion of non-ionized drug is available to cross the blood-brain barrier at lower pH (more acidic) in low perfusion states.62,63 Barbiturates are greatly bound to plasma proteins, particularly albumin. The amount of drug


crossing the blood-brain barrier is inversely proportional to its protein binding, thus unbound free drug affects the onset of action in CNS.64 The physiologic pH and disease states influence the degree of protein binding of a drug. The drug concentration is another factor proportionately regulating the drug transfer via the blood-brain barrier. The plasma concentration is determined by the dose given and the rate of administration. Lipid solubility, CSF drug concentration and degree of ionization influence the movement of drugs from the CSF to plasma. Since equilibrium between brain concentration and plasma concentration exists, the termination of the drug action is determined by the same factors which determine the rate of onset of barbiturate effects. Awakening from a single dose of thiopental takes 5 to 10 minutes after administration as the drug level in the brain decreases and gets redistributed from vastly perfused cerebral tissues to well-perfused muscles. In elderly patients, delayed awakening may be observed because of altered metabolism, increased CNS sensitivity to anesthetics and decreased central volume of distribution compared to younger adults.65 Rapid total clearance and shorter plasma thiopental clearance appears to manifest as early awakening in pediatric patients than adults despite multiple dosing.66 Uses and dosing of thiopentone is given in Table 12.2. Table 12.2: Uses and doses of thiopentone Induction of general anesthesia Adults: 3–5 mg/kg in healthy adults Children: 5–6 mg/kg Infants: 6–8 mg/kg Dose in status epilepticus

2–4 mg/kg Infusion: 1–5 mg/kg/hr

Side Effects The typical solution of thiopental (2.5%) is highly alkaline (pH=9) and can be irritating to the tissues, if injected extravenously. An urticarial rash may develop on the head, neck, and trunk that last a few minutes. More severe reactions, such as facial edema, hives, bronchospasm, and anaphylaxis, can also occur. Accidental administration of thiobarbiturates as an intra-arterial injection is a serious complication than can cause intense vasoconstriction, thrombosis, and even tissue necrosis due to formation of crystals in the arterioles and capillaries. Such injections should be treated without delay by maintaining the cannula and flushing it with saline, intra-arterial injections of papaverine and lidocaine (or procaine), as well as a sympathectomy (stellate ganglion block, brachial plexus block) and heparinization (to prevent thrombosis).


Essentials of Trauma Anesthesia and Intensive Care

Barbiturates cause dose-dependent respiratory depression especially exaggerated in COPD patients.67 Bronchospasm or laryngospasm following induction with thiopental is usually more than with propofol which is the result of airway manipulation in ‘lightly’ anesthetized patients. After induction, apnea occurs in at least 20% of cases for approximately 25 seconds.68 ‘Double apnea’ is observed after thiopental injection; with an initial apnea of few seconds during the drug administration which is followed by a few breaths and subsequently by a second lengthier apneic period. This warrants the airway to be secured often by controlled ventilation when using barbiturates. The cardiovascular effects of thiopental include decreases in systemic arterial pressure, cardiac output and peripheral vascular resistance. The depressant effects are consequent to a decrease in venous return due to a direct myocardial depressant effect (negative inotropic), peripheral pooling (vasodilatation) and a transiently decreased sympathetic outflow from CNS which is of great importance in the presence of hypovolemia and myocardial disease.69-71 Contraindications Respiratory compromise, severe hypotension (cardiovascular instability), status asthmaticus, porphyria may be precipitated or acute attacks may be accentuated by the administration of thiopental.72 Thiopental should not be administered in absence of proper equipment and airway instrumentation.73 Thiopental in Hemorrhagic Shock Thiopental causes exaggerated cardiovascular responses in presence of hypovolemia owing to the effects, like arteriolar vasodilation, negative inotropy and obtunded baroreceptor reflexes. It would be prudent to avoid thiopental in hypovolemic patients as there is a significant decrease in cardiac output (69%) and a significant lowering of blood pressure. Ketamine Ketamine is in clinical use since 1970. It is an arylcycloalkylamine, intravenous anesthetic agent unrelated to barbiturates, steroids, or phenolic agents but structurally related to phencyclidine.74,75 Ketamine differs from most other drugs used to induce anesthesia because it has a marked analgesic effect. It usually does not depress the cardiovascular and respiratory systems although it does possess some of the adverse psychological effects found

with the other phencyclidines. Additionally, it induces a state of sedation, immobility and amnesia (although the profundity of the amnesia varies) but the eyes remain open and many reflexes are maintained. Although corneal, cough, and swallowing reflexes may be present, they are not protective. Ketamine is water-soluble compound with a pKa of 7.5 available as solutions of 10, 50 and 100 mg/mL in an aqueous acidic (pH 3.5–5.5) solution containing a preservative. Despite a stable formulation, it should not be mixed with alkaline solutions, such as the barbiturates or with diazepam. Ketamine produces ‘dissociative anesthesia’ (functional dissociation between thalamocortical and limbic systems) comes from the feeling of strong dissociation from the environment that patients experience when this agent is administered. It depresses neuronal function in the cerebral cortex and thalamus, while simultaneously activating the limbic system, including the hippocampus.76 These effects appear to be related to its antagonistic activity at the NMDA receptor. It additionally binds to non-NMDA glutamate receptors and nicotinic, muscarinic, monoaminergic, and opioid receptors. Neuronal sodium channels (producing a modest local anesthetic action) and calcium channels (causing cerebral vasodilatation) are also inhibited by ketamine. Ketamine has rapid-onset/rapid-offset characteristics. It acts as an antagonist to CNS muscarinic receptors and as an agonist to opioid receptors. Although the S (+) stereoisomer is three to four times as potent (more potent anesthetic and analgesic) as the R (+) isomer, ketamine is marketed as a racemic mixture; the R (+) isomer has more side effects, including disturbing emergence reaction.77,78 Metabolism Ketamine is widely metabolized by hepatic microsomal cytochrome P-450 enzymes and its primary metabolite (by N-demethylation), norketamine, is one-third to one-fifth as potent as the parent compound. Norketamine metabolites are water-soluble hydroxylated and glucuronidated conjugates excreted by the kidneys.74 Ketamine has fairly short distribution and redistribution half-life. The high lipid solubility of ketamine is reflected in its large volume of distribution, nearly 3 L/kg. It also has a high hepatic clearance rate (1L/min), resulting in a short elimination half-life of 2 to 3 hours. The high hepatic extraction ratio suggests that changes in hepatic blood flow can significantly influence ketamine’s clearance rate. Ketamine may be given by

Intravenous Anesthetic Agents

alternative routes i.e. orally and via an intranasal spray and is subject to significant first-pass metabolism. The bioavailability via oral administration is 20 to 30%, and via the intranasal route is approximately 40 to 50%.79 Ketamine increases CMRO2, CBF and ICP.80,81 The use of thiopental82 or diazepam80,81 can block the increase in CMRO2 and CBF. Cerebrovascular responsiveness to carbon dioxide apparently seems to be preserved with ketamine; lowering PaCO 2 attenuates the increase in ICP after ketamine.80 The onset of action is within 30 to 60 seconds of administration with the maximal effect occurring in about 1 minute. Increase in the secretions, lacrimation, salivation, skeletal muscle tone and moderate dilatation of the pupils is observed after ketamine administration. Analgesia occurs at lower blood levels than loss of consciousness. Ketamine has been shown to inhibit nociceptive central hypersensitization.83 Ketamine also reduces acute tolerance after opiate administration.84 Ketamine is administered intravenously, intramuscularly, transcutaneously, orally, nasally and rectally, and as a preservative-free solution epidurally or intrathecally.85 Anesthetic induction doses of ketamine in patients premedicated with benzodiazepines is 1–2 mg/kg (intravenous) or 4–8 mg/kg (intramuscular). In pediatric patients, oral (3–10 mg/kg: onset varying from 20–45 mins) or intranasal ketamine (6 mg/kg) may be used as premedication prior to securing an intravenous cannulation. Uses and doses of intravenous ketamine are enumerated in Table 12.3. The induction time is usually within one armbrain circulation, i.e. less than 60 seconds. A sense of dissociation is usually evident within 15 seconds, and consciousness is lost within 30 seconds. After a single bolus (2 mg/kg), and assuming no other drugs have been administered, ketamine will have an offset time of 10 to 15 minutes for unconsciousness, about 40 minutes for Table 12.3: Uses and doses of intravenous ketamine Induction of general anesthesia premedicated with benzodiazepines in healthy adults

1–2 mg/kg IV 4–8 mg/kg IM 3–10 mg/kg oral (pediatric) 6 mg/kg (nasal)


0.2–0.8 mg/kg


0.5–2 mg/kg IV, 4–8 mg/kg IM


0.5–1 mg/kg ( with N2O 50% in O2)


0.1 to 0.5 mg/kg IV Infusion: 4 µg/kg/min IV Infusion: 75–200 µg/kg (opioid sparing, adjuvant)

Pre-emptive analgesia

0.15–0.25 mg/kg IV


analgesia, and as long as 1 to 2 hours for amnesia. Ketamine is used commonly for sedation (0.2–0.8 mg/kg IV over 2–3 min), induction (0.5–2 mg/kg IV, 4–6 mg/kg IM), and maintenance (0.5–1 mg/kg IV with N2O 50% in O2) of general anesthesia. Analgesic effects are evident at subanesthetic doses of 0.1 to 0.5 mg/kg IV. A low-dose infusion of 4 µg/kg/min IV was reported to result in equivalent postoperative analgesia as a morphine infusion of 2 mg/h IV. Opioid-sparing effects are noticed when low dose ketamine infusion of 75–200 µg/kg is administered as an adjuvant during anesthesia.86,87 Ketamine in smaller doses (0.15–0.25 mg/kg IV) plays an important role in pre-emptive analgesia and for the treatment or prevention of opiate tolerance and hyperalgesia. Complete orientation to person, place, and time occurs within 15 to 30 minutes and may require an additional 60 to 90 minutes. The relatively short duration of action of ketamine is due to its redistribution from the brain and blood to the other tissues in the body. The termination of effect after a single bolus administration of ketamine is caused by drug redistribution from the wellperfused to the less perfused tissues. Simultaneous administration of benzodiazepines, a common premedicant, may prolong the effect of ketamine.88 Ketamine in subanesthetic dose (30 breaths/minute)


Cumulative score >5 required for diagnosis

events is suggestive of FES.186 Other non-specific laboratory findings are anemia, thrombocytopenia and raised ESR. Anemia has been attributed to intra-alveolar hemorrhage. Presence of fat globules in urine, blood and sputum may be seen, although not considered as sensitive tests. Chest roentgenograms reveal bilateral diffuse pulmonary infiltrates (snow storm appearance). Dilatation of right heart will be seen. Computed tomogram (CT) head may be normal or show diffuse white matter petechial hemorrhages in patients with cerebral fat embolism (CFE). Spiral CT chest may be normal or show features suggestive of lung contusion, acute

The management of FES primarily remains supportive.165,177,178 Maintaining adequate oxygenation, ventilation, intravascular volume and stable hemodynamics and blood transfusion as indicated remains the mainstay of medical therapy.188 Volume resuscitation may be achieved with albumin, which gives blood volume restoration and also binds with free fatty acid, thus decreasing the extent of lung injury.177,181 If required, mechanical ventilation with PEEP should be given; or use of prone position ventilation should be considered.178 Percutaneous cardiopulmonary bypass has also been used intraoperatively in patients sustaining catastrophic pulmonary fat embolism resulting in cardiac arrest, during intramedullary nailing of femur. Corticosteroids have been recommended by few authors for the management of the FES.177 An antiinflammatory effect decreasing the perivascular hemorrhage and edema is the proposed mechanism. However, there is not enough data to support initiating steroid therapy once FES is established. No beneficial effect was demonstrated in an experimental study, and there have been no prospective, randomized, and controlled clinical trials demonstrating significant beneficial effects with their use. Since FES is associated with 5–15% mortality, early fixation of long bones within 24 hours is essential to prevent fat embolism.165,176,177 Frequent and thorough clinical assessments, and monitoring the pulmonary and neurological systems is essential for early diagnosis of FES to prevent complications. All patients at risk for FES should have continuous oxygen saturation monitoring. Unreamed nailing and smaller-diameter nails have been found to be useful in the prevention of FES. Fixation with plate and screws has been shown to produce less lung injury than intramedullary nailing.189 Preoperative use of methylprednisolone may prevent the occurrence of FES, although controversial, mainly because it is difficult to definitively prove beneficial effects in a low incidence condition with a low mortality, and usually a positive outcome with conservative management. Despite that, many studies have demonstrated decreased incidence and severity of FES with prophylactic


Essentials of Trauma Anesthesia and Intensive Care

administration of corticosteroids.188,190 Sixty-four patients with lower-limb long-bone fractures were studied in a double-blind randomized study; either placebo or methylprednisolone, 7.5 mg/kg every 6 h for 12 doses were administered in both the groups.185 9 of 41 placebo-treated patients were diagnosed to have FES while none of the steroid-treated patients (P 10% in 47% patients, while it decreased in 31%, and remained unchanged in the rest 22% patients.46 Administration of volume also increased right atrial pressure and the left ventricular end diastolic pressure (LVEDP). The authors suggested that fluid administration increases CO in 50% patients with cardiac tamponade, and systolic BP 95%

In the presence of a pulmonary catheter Pulmonary capillary wedge pressure

6–10 mm Hg

Cardiac index

2.4 liter min-1/m-2

Systemic vascular resistance


(Adapted with permission from McKeown DW, Bonser RS, Kellum JA. Management of the heartbeating brain dead organ donor. Br J Anaesth 2012 Jan 1;108 (suppl 1):i96–i107)


Essentials of Trauma Anesthesia and Intensive Care

Management of Blood Pressure The management of blood pressure in the brain dead potential organ donor is challenging; because it involves the treatment of both hypertensive and hypotensive states. Both the Brazilian and Canadian guidelines recommend that systemic hypertension, which is severe and prolonged, after neurological determination of death needs to be treated.31,60 The recommended treatment thresholds are:

• SBP >160 mm Hg; and/or • MAP >90 mm Hg; • Autonomic storm of severe degree (systolic >180 mm Hg; diastolic >100 mm Hg; or mean >90 mm Hg) and prolonged (>30 to 60 minutes) Preferred therapy: Short-acting agents are preferred, since longer-acting drugs may aggravate the hypotension which follows. The preferred drug therapy is:

• Nitroprusside, 0.5–5.0 µg/kg/minute; and/or • Esmolol, 100–500 µg/kg bolus followed by 100–300 µg/kg/minute Infusions should be titrated until the desired clinical effect is achieved. Hypotension has multifactorial origin in the brain dead patient as already discussed in pathophysiology. It is recommended to maintain the MAP over 65–70 mm Hg and the SBP above 100 mm Hg, by optimizing volume status and starting inotropic drugs, if not responding to fluids.60,62 The objective of fluid resuscitation is to improve tissue perfusion, inhibit systemic inflammatory activation and ensure organ quality. At the same time, excessive fluid administration causing acute pulmonary edema and, therefore, compromising lung viability for transplantation must be avoided. So, both too little and too much fluid is detrimental in the potential organ donor. Adequate and accurate hemodynamic monitoring is, therefore, a must to ensure controlled volume repletion and to avoid iatrogenic fluid overload.25 Restrictive fluid therapy does not have adverse effect on donor organs, if appropriate monitoring has been done. Volume repletion for pressure stabilization must begin with 20 to 30 mL/kg of warm crystalloid solution (43°C) over 30 minutes. Further infusions should be guided by oxygenation and metabolic parameters. There is no proven advantage of using colloid solutions (e.g. 6% HES) in volume resuscitation. They have been implicated in renal tubular damage and impaired early graft function. Inotropic or

vasopressor agent infusions should be started only after this fluid loading has been done. If the MAP is less than 40 mm Hg or SBP is less than 70 mm Hg, a vasopressor agent can be started before the completion of or simultaneously with the crystalloid infusion. Indiscriminate use of vasopressors should be avoided as it may lead to deterioration with arrhythmias, aggravation of hypotension (if dobutamine is used) or exacerbation of vasoconstriction leading to multiple organ ischemia. The Canadian guidelines recommend vasopressin as the first line agent for hemodynamic support.31 It can be used with a 1 IU initial bolus followed by continuous infusion from 0.5 to 2.4 IU/h. The maximum dose should be 2.4 U/h (0.04 U/minute). Catecholamine infusions can be gradually discontinued once blood pressure stabilizes after the vaso-pressin infusion. Vasopressin proves to be advantageous due to its variety of applications, i.e. hemodynamic vaso-pressor support, diabetes insipidus therapy and hormonal therapy. However, there are no randomized studies to establish the efficacy of vasopressin over other vasopressors in organ donors.31,60 Norepinephrine, epinephrine and/or phenylephrine can also be used for hemodynamic support. The dose should be titrated to clinical effect (MAP >65 mm Hg, SBP >100 mm Hg). There is no predetermined upper limit but dose of norepinephrine beyond 0.05 mg/kg/min should be used with caution, since it is associated with increased cardiac graft dysfunction and higher mortality in recipients. If there are any signs of impairment of heart rate or signs of hypoperfusion with no clinical evidence of ventricular dysfunction or an ejection fraction 55 years of age or a female >60 years, or a male >40 years of age or a female >45 years in the presence of two risk factors or presence of three or more risk factors at any age or there is a history of cocaine use. Cardiovascular risk factors for coronary artery disease that impact transplant outcomes include smoking, hypertension, diabetes, hyperlipidemia, body mass index (BMI) >32 kg/ m2 family history of the disease, prior history of coronary artery disease, ischemia on ECG, anterolateral regional wall motion abnormalities on echocardiogram, two-dimensional echocardiographic assessment of ejection fraction of 80 mm Hg, PaCO2 35– 45 mm Hg) MAP >70 mm Hg (dopamine 0.1 µg/kg


Heart retrieval

Hormonal therapy • • • •

Desmopressin IV 1–4 µg/day in 1–2 doses T4 IV 20 µg, initial dose →10 µg/h continuous infusion Steroids IV prednisolone 15 mg/kg/day Insulin infusion to maintain blood sugar 120–180 mg/dL

Hemodynamic assessment • • • • • •

MAP >70 mm Hg CVP >6–10 mm Hg PAWP 8–12 mm Hg CI 2.4 L/m2 SVR 800–1200/dyne/cm5 Reduced doses of vasoconstrictors and catecholamines after 2 h of ECHO observation

EF >45%

Heart retrieval

EF 90 mm Hg and SaO2 >95%

• • • • •

Humidification and warming of respiratory gases Positioning—semi-recumbent 30–45º Sealing of the cuff >25 cm H2O Frequent aspiration of oral secretions Aspiration of bronchial tree secretions in the closed system Alveolar recruitment maneuvers after each disconnection of the system Chest X-ray Methylprednisolone 15 mg/kg Tracheal aspirate—bacteriological tests Bronchoscopy—BAL Broad spectrum antibiotic therapy

• • • • • •

PaO2 300 Qualification

• • • • • •

Correction of ETT position Lateral decubitus position—physiotherapy Alveolar recruitment (PEEP 10–15 cm H2O; PIP up to 30 cm H2O) Negative fluid balance (diuretics, crystalloid restriction, albumins for vascular bed filling, CVP–6 mm Hg) Chest X-ray Arterial blood gas

Chest X-ray bilateral infiltrations,

Chest X-ray unilateral infiltrations,

Chest X-ray no infiltrations,


PaO2:FiO2 >300

Abandonment of retrieval

Qualification of one lung

Qualification of both lungs

Fig. 34.14: Protocols for management of the potential lung donor VT: tidal volume; PEEP: positive end-expiratory pressure; RR: respiratory rate; BAL: bronchioalveolar lavage; ETT: endotracheal tube; PIP: peak inspiratory pressure; CVP: central venous pressure · (Adapted from Kucewicz E, Wojarski J, Zegle´ n S, Saucha W, Maciejewski T, Pacholewicz J, et al. The protocols of multi-organ donor management. Anesthesiol Intensive Ther 2009;XLI(4):205–11)

Organ Donation After Brain Death Table 34.7: Mechanical lung ventilation in potential donors—lung protective strategies Ventilator parameters Volume-controlled ventilation mode •

VT 6–8 mL/kg

PEEP 8–10 cm H2O

Frequency adjusted to PaCO2 40–45 mm Hg

FiO2 adjusted to maintain PaO2 >90 mm Hg

Secretion aspiration •

Every 4–6 hours

Closed system suction catheters

Alveolar recruitment maneuvers •

After each disconnection of the ventilator system

10 breaths 2 × VT

Apnea test •

Without ventilator disconnection, CPAP equal to PEEP during ventilation

FiO2 0.60

VT : Tidal volume; PEEP: Positive end expiratory pressure; CPAP: Continuous positive airway pressure

inflated with pressures of over 25 cm H2O. The volume controlled mode is usually used. Pressure-controlled ventilation with set pressure of 25 cm H2O and PEEP of 15 cm H2O has been used in patients with low oxygenation ratios (PaO2:FiO2) and lung infiltrates. Serial ABGs, lung X-rays and bronchoscopies are done as part of respiratory management. Bronchoscopy should be done early by experienced personnel. Bronchial lavage samples should be sent for bacteriological tests. Gram stain or culturesensitivity-guided antibiotic therapy should be instituted in patients suspected of or with confirmed bronchopneumonia. In patients at high risk for pneumonia, empirical broadspectrum antibiotic therapy can be initiated. Intravenous fluid therapy should follow a restrictive pattern with the aim of achieving a negative balance. 20% albumin can be used to supplement vascular volume.25 The presence of abundant purulent secretions in the bronchial tree which cannot be completely removed by bronchoscopy is a reason for disqualification of the lungs for organ retrieval. Other contraindications for retrieval are persistent bilateral infiltrations on X-ray despite intensive therapy. The non-diseased lung can be retrieved in the presence of unilateral infiltrates.25 The PaO2:FiO2 ratio >300 is the main criterion for deciding whether the lungs can be retrieved. The surgeon does a direct assessment of lungs in the surgical field and then makes the final decision for retrieval.25


Liver All potential liver donors are assessed for history of jaundice, hepatitis and excessive alcohol ingestion. Liver enzyme (SGOT and SGPT) levels, bilirubin (direct and indirect where available) levels and INR PT, repeated every 6 hours must be available. Serum electrolytes, creatinine, urea hepatitis B surface antigen (HBsAg), hepatitis B core antibody (HBcAb), hepatitis C virus antibody (HCVAb) also need to be done. There are no upper limits to the values of SGPT and SGOT recommended that contraindicate transplantation. It is recommended to offer all livers for transplant. Whether the organ is transplantable depends upon organ status, trends in liver function over time and recipient status. Hepatic ultrasound is not required in all patients. Percutaneous ultrasound-guided liver biopsy is indicated in donors with body weight >100 kg, or BMI >30 kg/m2 or HCV Ab positivity. It can be done when a procurement team is not available immediately, i.e. a distant procurement. Intraoperative liver biopsy is recommended in all other instances where liver biopsy is indicated. If a liver biopsy is indicated but not available or possible, then the transplantation of the liver is dependent upon the discretion of the liver transplantation team.31 Kidney Abnormal serum creatinine levels or creatinine clearance alone is not an absolute contraindication to renal graft procurement. The optimum function threshold for renal function for transplantation is a creatinine clearance rate of >80 mL/minute/1.73 m2. Urinalysis is necessary to rule out kidney abnormalities. Six hourly measurements of serum creatinine and blood urea nitrogen must be done. The decision to perform a renal US scan is taken on a patient to patient basis. This investigation does not provide much information and there are no firm indications for it. Intraoperative biopsies should be done in donors aged over 65 years or those younger but with a history of creatinine level >1.5 mg/dL, hypertension, diabetes or abnormal urinalysis. Glomerulosclerosis and vasculopathy should be ruled out before retrieving kidneys. Biopsies should be done during organ procurement and not in the ICU.31 OTHER CONSIDERATIONS Optimal Time for Organ Procurement A time period within 12 to 24 hours following diagnosis is considered adequate for the optimization of the brain dead


Essentials of Trauma Anesthesia and Intensive Care

organ donor. The adoption of uniform aggressive protocols during this period reduces losses resulting from hemodynamic instability in 87%, increasing the total donor number by 19%, actual donors by 82%, and effective donations by 71%.31,60,82 Decisions Regarding Transplantability The final decision rests upon the transplantation team. It is recommended that all organs be offered for transplant as per the legal and regulatory frameworks available. Organ Retrieval Two principles must always be upheld during an organ retrieval procedure:83 1. The warm ischemia time should be kept as minimum as possible as this is the period during which metabolic processes will be continuing in an anoxic state. 2. The donated organs must be retrieved without any injury or damage. These surgeries are, therefore, more precise and exacting than those performed to remove a diseased organ in the living. The advantage of donation after brain death is that the heart is beating and the intrathoracic and intra-abdominal organs are perfused with oxygenated blood right up to the point of procurement. Hence, the incidence of warm ischemic injury to the organ prior to removal is minimal. MANAGEMENT IN OPERATING ROOM One brainstem dead can donate multiple organs and save many lives; hence there are multiple patients on the table to be managed. Many staff members would be present during the organ retrieval process, thus crowding the OR and making the procedure difficult for all. Hence, the biggest OR should be used. All the team members, including the anesthesiologist should check the legal documents prior to commencement of the procedure. The primary role of an anesthesiologist is to maintain optimal perfusion and protect the organs by maintaining hemodynamic status and exchange of gases and maintaining normal body temperature till the aorta cross-clamped. This can be challenging; hence, ideally anesthetic support is provided by an appropriately experienced anesthesiologist.84 The goals of intraoperative management of the respiratory, cardiovascular, hematologic and neurologic systems are identical to those in the ICU. All the supportive treatment is continued in the OR. A broad guide for anesthetic management of the brain dead donor is

the ‘rule of 100’: SBP >100 mm Hg, urine output >100 mL/ h, PaO2 >100 mm Hg and Hb concentration >100 g/liter. A blood sugar level of 100% normal was added later.28,85 Mechanical ventilation settings are the same as those in the ICU. FiO2 of 100% should be used until the first ABG result is available except in cases where procurement of the lungs or the heart-lungs is anticipated. In these patients, FiO2 should not exceed 40%. The EtCO2 should be maintained between 30 and 35 mm Hg. All standard monitorings are required including invasive hemodynamic monitoring. If femoral artery has been cannulated, it is preferable to perform radial artery cannulation. Hourly ABGs, Hb/hematocrit, serum electrolytes and glucose monitoring must be done. In the heart-lung or lung donor, ABG analysis should be done every half hourly. One may believe that brainstem patients do not require analgesia or sedation during surgery for multiorgan procurement. But, both visceral and somatic reflexes can lead to physiologic responses during the procedure. These can include reflex muscle contraction and hypertension. The chances of many anesthesiologists being uncomfortable in this situation are quite high. This could be because it is rare for us to perform a surgery without analgesia or anesthesia to the point that there is a psychological compulsion to provide anesthesia. The reflex hypertension and tachycardia can reach levels distressing for the OR personnel to witness and anesthesia should be administered to counter these reflexes. The mean blood pressure increase during this procedure is 31 mm Hg and mean heart rate increase is to the tune of 23 beats/min.86 This has been attributed to spinal reflexes, which can occur spontaneously or on surgical stimulus.87 Even a brain dead with liquefied cortex may demonstrate cardiovascular changes, and these are due to spinal reflexes. They are generated as well as modifiable at spinal cord level itself.88 We must always remember that our understanding of the process of death is limited. Therefore, it is better to err on the side of caution and provide anesthesia.89 Control of reflex hypertensive responses to surgical stimulation may require the tapering off of vasopressor and inotropic support and institution of vasodilator therapy with sodium nitroprusside or nitroglycerin or inhalational agents, e.g. isoflurane. Volatile anesthetic agents have also shown to induce ischemia preconditioning in hepatic and cardiac surgery.90,91 Hence, it is administered during the last 30 minutes prior to aortic clamping by some retrieval teams.92 Neuromuscular relaxation should be given at the beginning of the procedure and supplemented as required

Organ Donation After Brain Death


to eliminate reflex neuromuscular activity and to facilitate surgical retraction. A long-acting neuromuscular agent, like pancuronium, may be preferred.93 Many pharmacological interventions may be required to ensure organ preservation. Dopamine (2–3 mg/kg/min), furosemide, mannitol, allopurinol (free-radical scavenger), chlorpromazine and phentolamine (vasodilators), heparin (prevents microvascular thrombosis and promotes reperfusion), and prostaglandin E1 (PGE1) (vasodilator, membrane stabilizer, antiplatelet effect) can be used as necessary. Systemic infusion of PGE1 prior to aortic cross-clamping (commonly used in heart-lung or lung procurement) will lead to predictable and profound fall in blood pressure. Hemodynamic instability may be observed during handling of the heart and placement of slings around the inferior vena cava and aorta. Volume resuscitation towards optimal CVP should continue until the aortic cross-clamp is applied. Large volumes may be required to replace significant third space losses. MAP should be maintained between 60 and 70 mm Hg. Vasopressors may be required in patients unresponsive to fluid therapy. A catheter should be used after verifying the ability to freely aspirate blood, if intravenous heparin is to be given. Methylprednisolone (30 mg/kg) is commonly administered at least 2 h before organ retrieval in an effort to protect the heart and kidneys from ischemic injury.93

Anticoagulation with unfractionated heparin (300 IU/ kg) is given 3 minutes before aortic cross-clamping. Anesthesia care continues until the proximal aortic crossclamp is applied. At this point, all monitoring and supportive therapies are discontinued. When the lung or the heart-lung is to be retrieved, all monitorings except FiO2 are stopped with aortic cross-clamping. All supportive care is stopped. Mechanical ventilation, though, is continued at 4 breaths/ min or as desired by the transplant team. Suctioning of the endotracheal tube is done just prior to the removal of the tube. Extubation is the end point of anesthetic care of the heart-lung or lung donor.93

Blood transfusions should be given as per donor management guidelines to maintain Hb >8 gm% after discussing with the surgical team. In case the donor is relatively stable and the procedure is almost complete, it is better to accept lower Hb than adding potential risks of transfusion.

Popular preservative solutions used are University of Wisconsin (UW), solution, hyperosmolar citrate (HOC), histidine-tryptophan-ketoglutarate (HTK), Celsior, ViaSpan and Perfadex. The duration of preservation in donation after cardiac donation organs and type of preservation solution used in clinical practice is given in Table 34.8.83

During heart-lung procurement, mediastinal and tracheal dissection and manipulation of the lung outside the mediastinum may cause a sudden large fall in blood pressure. Problems with oxygenation and ventilation can occur and must be communicated to the transplant team immediately. The position of the endotracheal tube must be checked and it must be ensured that there is no chance of the tube causing mucosal injury at the site of the anticipated suture line. Complications that have to be anticipated and treated include hypotension, dysrhythmias, cardiac arrest, oliguria, diabetes insipidus, coagulopathy, hyperglycemia and hypothermia. These are managed as per donor management guidelines. Desmopressin should be discontinued at least one hour prior to aortic cross-clamping.93

Duration of the entire procedure is dependent upon the surgical technique used. Usually the organs are dissected in situ and then cold preservative solutions perfused. Organs are then removed. This takes about four hours. If the ‘rapidflush technique’ is used, minimal dissection of the individual organs is done, and an en-bloc resection is done following aortic cross-clamping and perfusion of cold preservative. The organs are dissected ex-vivo, often at the transplant center. This technique results in shorter operating times averaging around 1.5 hours. Anticipated blood loss is around 200 mL. The heart is the first organ to be retrieved followed by the lungs. Liver and pancreas are removed next, then the kidneys and intestines. The corneas and bones are removed last.

Table 34.8: Duration of preservation in donation after cardiac donation organs and type of preservation solution used in clinical practice Organ

Duration of preservation (hours)

Preservation solution



UW, Celsior



UW, Celsior, Perfadex












(Reproduced with permission from Bagul A, Hosgood SA. Organ retrieval and preservation. Surg Oxf. 2011;29(7):306– 11)


Essentials of Trauma Anesthesia and Intensive Care

HANDING OVER THE PATIENT Once the organs have been retrieved, the incisions are sutured and closed. The endotracheal tube is removed (if not already removed in cases of lung or heart-lung retrieval) and so are the arterial and central venous or pulmonary arterial pressure catheters. The urinary catheter is also removed. The body is handed over to the family and relatives from the OR itself. SUMMARY It is the responsibility of the entire organ donation and retrieval team to ensure that the retrieval of precious organs result in successful organ transplantation. While we have made a lot of progress in the management of the brain dead organ donor since the first attempts were made in animals, further research is required and is continuing in all areas of management. REFERENCES 1. Demikhov V. Experimental transplantation of an additional heart in the dog. Bull Exp Biol Med Russ 1950;1:241. 2. Carrel A, Guthrie C. The transplantation of vein and organs. Am Med 1950;10:101. 3. Hoffenberg R. Christiaan Barnard: His first transplants and their impact on concepts of death. Br Med J 2001;323:1478. 4. Cooley D, Bloodwell R, Hallman G. Cardiac transplantation for advanced acquired heart disease. J Cardiovasc Surg Torino 1968;9:403–13. 5. Cooley DA, Hallman GL, Bloodwell RD, Nora JJ, Leachman RD. Human heart transplantation: Experience with twelve cases*. Am J Cardiol 1968;22:804–10. 6. Reitz BA, Wallwork JL, Hunt SA, et al. Heart-lung transplantation: Successful therapy for patients with pulmonary vascular disease. N Eng J Med 1982;306:557. 7. Determination of Death Act Summary [Internet]. [cited 2014 Aug 23]. Available from: Summary.aspx?title= Determination%20 of% 20 Death%20Act (Accessed on 03-09-2015). 8. Wijdicks EF, Varelas PN, Gronseth GS, Greer DM. Evidencebased guideline update: Determining brain death in adults Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2010;74:1911–18. 9. Diagnosis of brain death. Statement issued by the honorary secretary of the Conference of Medical Royal Colleges and their Faculties in the United Kingdom on 11 October 1976. Br Med J 1976;2:1187–88. 10. Criteria for the diagnosis of brainstem death. Review by a working group convened by the Royal College of Physicians and endorsed by the Conference of Medical Royal Colleges and their Faculties in the United Kingdom. J R Coll Physicians Lond 1995;29: 381–82.

11. Organ Retrieval Banking Organisation[Internet]. [cited 2014 Jun 23]. Available from: 12. Ministry of Law, Justice and Company Affairs (Legislative Department). The Transplantation of Human Organs (Amendment) Act, 2011 No.16 of 2011, 2011. 13. Williams M, Bell MDD, Moss E. Brainstem death. Contin Educ Anaesth Crit Care Pain 2003;3:161–66. 14. Walker AE, Diamond EL, Moseley J. The Neuropathological Findings in Irreversible coma: A Critique of The “Respibator Brain”. J NeuropatholExpNeurol [Internet] 1975;34 (4). Available from: THE_NEUROPATHOLOGICAL_ FINDINGS_IN _IRREVERSIBLE.1.aspx 15. Bugge JF. Brain death and its implications for management of the potential organ donor. Acta Anaesthesiol Scand 2009;53: 1239–50. 16. Novitzky D. Detrimental effects of brain death on the potential organ donor. Transplantation proceedings. Elsevier 1997; 3770–72. 17. Tuttle-Newhall JE, Collins BH, Kuo PC, Schoeder R. Organ donation and treatment of the multi-organ donor. Curr Probl Surg 2003;40:266–310. 18. Novitzky D, Rhodin J, Cooper DKC, Ye Y, Min KW, DeBault L. Ultrastructure changes associated with brain death in the human donor heart. Transpl Int 1997;10:24–32. 19. Dujardin KS, McCully RB, Wijdicks EF, Tazelaar HD, Seward JB, McGregor CG, et al. Myocardial dysfunction associated with brain death: Clinical, echocardiographic, and pathologic features. J Heart Lung Transplant 2001;20:350–57. 20. Shivalkar B, Van Loon J, Wieland W, Tjandra-Maga TB, Borgers M, Plets C, et al. Variable effects of explosive or gradual increase of intracranial pressure on myocardial structure and function. Circulation 1993;87:230–39. 21. Takada M, Nadeau KC, Hancock WW, Mackenzie HS, Shaw GD, Waaga AM, et al. Effects of Explosive Brain Death on Cytokine Activation of Peripheral Organs in the Rat1. Transplantation [Internet]. 1998;65(12). Available from: http:// EFFECTS_OF_ EXPLOSIVE_BRAIN_DEATH_ ON_ CYTOKINE. 1.aspx 22. Pratschke J, Wilhelm M, Kusaka M, Hancock W, Tilney N. Activation of proinflammatory genes in somatic organs as a consequence of brain death. Transplant Proc 1999;31:1003–65. 23. Avlonitis VS, Wigfield CH, Kirby JA, Dark JH. The hemodynamic mechanisms of lung injury and systemic inflammatory response following brain death in the transplant donor. Am J Transplant 2005;5:684–93. 24. Novitzky D, Wicomb WN, Rose AG, Cooper DKC, Reichart B. Pathophysiology of pulmonary edema following experimental brain death in the Chacma baboon. Ann Thorac Surg 1987;43: 288–94. 25. Kucewicz E, Wojarski J, Zegle´nS, Saucha W, Maciejewski T, Pacholewicz J, et al. The protocols of multi-organ donor management. Anaesthesiol Intensive Ther 2009;XLI:205–11.

Organ Donation After Brain Death 26. Barklin A. Systemic inflammation in the brain-dead organ donor. Acta Anaesthesiol Scand 2009;53:425–35. 27. McKeating EG, Andrews PJ. Cytokines and adhesion molecules in acute brain injury. Br J Anaesth 1998;80:77–84. 28. McKeown DW, Bonser RS, Kellum JA. Management of the heartbeating brain-dead organ donor. Br J Anaesth 2012;108: i96–i107. 29. Kosieradzki M, Kuczynska J, Piwowarska J, WegrowiczRebandel I, Kwiatkowski A, Lisik W, et al. Prognostic significance of free radicals: Mediated injury occurring in the kidney donor. Transplantation [Internet] 2003;75(8). Available from: http:// Prognostic_significance_of_free_radicals__ mediated.35.aspx 30. Koo DDH, Welsh KI, Mclaren AJ, Roake JA, Morris PJ, Fuggle SV. Cadaver versus living donor kidneys: Impact of donor factors on antigen induction before transplantation. Kidney Int 1999;56:1551–59. 31. Shemie SD, Ross H, Pagliarello J, Baker AJ, Greig PD, Brand T, et al. Organ donor management in Canada: Recommendations of the forum on Medical Management to Optimize Donor Organ Potential. Can Med Assoc J 2006;174:S13–S30. 32. Ghuge PP, Kute VB, Vanikar AV, Gumber MR, Gera DN, Patel HV, et al. Successful renal transplantation from a brain dead deceased donor with head injury, disseminated intravascular coagulation and deranged renal functions. Indian J Nephrol 2013;23:448. 33. Kaur M, Lalwani S, Gupta B, Vij A, Balakrishnan I, Sawhney C. Organ retrieval and banking in brain dead trauma patients: Our experience at level-1 trauma center and current views. Indian J Anaesth 2013;57:241. 34. Goila AK, Pawar M. The diagnosis of brain death. Indian J Crit Care Med Peer-Rev Off Publ Indian Soc Crit Care Med 2009;13: 7–11. 35. Oram J, Murphy P. Diagnosis of death. Contin Educ Anaesth Crit Care Pain 2011;11:77-81. 36. Wijdicks EF, Varelas PN, Gronseth GS, Greer DM. Evidencebased guideline update: Determining brain death in adults Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2010;74:1911–18. 37. Shlugman D, Parulekar M, Elston J, Farmery A. Abnormal pupillary activity in a brainstem-dead patient. Br J Anaesth 2001;86:717–20. 38. Young GB, Shemie SD, Doig CJ, Teitelbaum J. Brief review: The role of ancillary tests in the neurological determination of death. Can J Anesth 2006;53:620–27. 39. Saposnik G, Rizzo G, Vega A, Sabbatiello R, Deluca JL. Problems associated with the apnea test in the diagnosis of brain death. Neurol India 2004;52:342. 40. Goudreau J, Wijdicks E, Emery S. Complications during apnea testing in the diagnosis of brain death: Predisposing factors. Neurology 2000;55:1045–48. 41. Wijdicks EFM, Rabinstein AA, Manno EM, Atkinson JD. Pronouncing brain death: Contemporary practice and safety of the apnea test. Neurology 2008;71:1240–44.


42. Guideline three: Minimum technical standards for EEG recording in suspected cerebral deaths. American Electroencephalographic Society. J Clin Neurophysiol 1994;11:10–13. 43. Practice parameters for determining brain death in adults (summary statement). The quality standards subcommittee of the American Academy of Neurology. Neurology 1995;45: 1012–14. 44. Braun M, Ducrocq X, Huot J-C, Audibert G, Anxionnat R, Picard L. Intravenous angiography in brain death: Report of 140 patients. Neuroradiology 1997;39:400–05. 45. Munari M, Zucchetta P, Carollo C, Gallo F, De Nardin M, Marzola MC, et al. Confirmatory tests in the diagnosis of brain death: Comparison between SPECT and contrast angiography. Crit Care Med [Internet] 2005;33(9). Available from: http:// in_the_diagnosis_of_brain.26.aspx 46. Tatlisumak T, Forss N. Brain death confirmed with CT angiography. Eur J Neurol 2007;14:e42–e43. 47. Taylor T, Dineen RA, Gardiner DC, Buss CH, Howatson A, Pace NL. Computed tomography (CT) angiography for confirmation of the clinical diagnosis of brain death. Cochrane Database Syst Rev 2014 (Issue 3). 48. Orrison WW, Champlin AM, Kesterson OL, Hartshorne MF, King JN. MR ‘hot nose sign’ and ‘intravascular enhancement sign’ in brain death. Am J Neuroradiol 1994;15:913–16. 49. Ishii K, Onuma T, Kinoshita T, Shiina G, Kameyama M, Shimosegawa Y. Brain death: MR and MR angiography. Am J Neuroradiol 1996;17:731–35. 50. Monteiro LM, Bollen CW, Huffelen AC, Ackerstaff RGA, Jansen NJG, Vught AJ. Transcranial Doppler ultrasonography to confirm brain death: A meta-analysis. Intensive Care Med 2006;32:1937– 44. 51. Meyer M. Evaluating brain death with positron emission tomography: Case report on dynamic imaging of 18Ffluorodeoxyglucose activity after intravenous bolus injection. J Neuroimaging 1996;6:117. 52. Medlock M, Hanigan W, Cruse R. Dissociation of cerebral blood flow, glucose metabolism, and electrical activity in pediatric brain death. J Neurosurg 1993;79:752. 53. Waters CE. Difficulty in brainstem death testing in the presence of high spinal cord injury. Br J Anaesth 2004;92:760–64. 54. Andrews KM, Lesley Munday, Ros Littlewood, Clare. Misdiagnosis of the vegetative state: Retrospective study in a rehabilitation unit. Br Med J 1996;313:13–16. 55. Jellinger KA. Brain Death and the Vegetative State.eLS [Internet]. John Wiley and Sons, Ltd; 2001. Available from: 10.1002/9780470015902.a 0002212.pub2 56. Byrne P, Canadian Pediatric Society (CPS), Bioethics Committee. Use of anencephalic newborns as organ donors. Paediatr Child Health 2005;10:335–37. 57. Religion, organ transplantation, and the definition of death. The Lancet 2011;377:271.


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58. Oliver M, Woywodt A, Ahmed A, Saif I. Organ donation, transplantation and religion. Nephrol Dial Transplant 2011;26: 437–44.

Martiner AC, et al. An under-recognized benefit of cardiopulmonary resuscitation: Organ transplantation. Crit Care Med 2013;41:2794–99.

59. Acharya V. Status of renal transplant in India—May 1994. J Postgrad Med 1994;40:158–61.

71. Magliocca JF, Magee JC, Rowe SA, Gravel MT, Chenault RH, Merion RM, et al. Extracorporeal support for organ donation after cardiac death effectively expands the donor pool. J Trauma Inj Infect Crit Care 2005;58:1095–102.

60. Westphal GA, Caldeira Filho M, Fiorelli A, Vieira KD, Zaclikevis V, Bartz M, et al. Guidelines for maintenance of adult patients with brain death and potential for multiple organ donations: The Task Force of the Brazilian Association of Intensive Medicine the Brazilian Association of Organs Transplantation, and the Transplantation Center of Santa Catarina. Transplant Proc 2012;44:2260–67. 61. Keegan MT, Wood KE, Coursin DB. An update on ICU management of the potential organ donor. In: Vincent JL, editor. Yearbook of Intensive Care and Emergency Medicine 2010 [Internet]. Springer Berlin Heidelberg; 2010; 547–59. Available from: (Accessed on 03-09-2015). 62. Ramos HC, Lopez R. Critical care management of the brain dead organ donor. CurrOpin Organ Transplant [Internet]. 2002;7(1). Available from: Fulltext/2002/03000/Critical_care_management_of_the_ brain_dead_ organ.15.aspx. (Accessed on 03-09-2015). 63. Yoshioka T, Sugimoto H, Uenishi M, Sakamoto T, Sadamitsu D, Sakano T, et al. Prolonged hemodynamic maintenance by the combined administration of vasopressin and epinephrine in brain death: A clinical study. Neurosurgery [Internet]. 1986;18(5). Available from: 1986/05000/Prolonged_Hemodynamic_ Maintenance_ by_the_ Combined.9.aspx 64. Powner DJ, Doshi PB. Central venous oxygen saturation monitoring:Role in adult donor care? Prog Transplant 2010; 20:401–06. 65. MOnIToR Study. Clinical Trial [Internet]. [cited 2014 Aug 20]. Available from: asp?logged=0 66. Al-Khafaji A, Murugan R, Wahed AS, Lebovitz DJ, Souter MJ, Kellum JA. Monitoring organ donors to improve transplantation results (monitor) trial methodology. Crit Care Resusc 2013; 15:234. 67. Cinotti R, Roquilly A, Mahé P-J, Feuillet F, Yehia A, Belliard G, et al. Pulse pressure variations to guide fluid therapy in donors: A multicentric echocardiographic observational study. J Crit Care 2014;29:489–94. 68. Casartelli M, Bombardini T, Simion D, Gaspari MG, Procaccio F. Wait, treat and see: Echocardiographic monitoring of brain dead potential donors with stunned heart. Cardiovasc Ultrasound 2012;10:25. 69. Vedrinne JM, Vedrinne C, Coronel B, Mercatello A, Estanove S, Moskovtchenko JF. Transesophageal echocardiographic assessment of left ventricular function in brain dead patients: Are marginally acceptable hearts suitable for transplantation? J Cardiothorac Vasc Anesth 1996;10:708–12. 70. Orioles A, Morrison WE, Rossano JW, Shore PM, Hasz RD,

72. Hsieh CE, Lin HC, Tsui YC, Lin PY, Lin KH, Chang YY, et al. Extracorporeal membrane oxygenation support in potential organ donors for brain death determination. Transplant Proc 2011;43:2495–98. 73. Bajwa SJ, Haldar R. Brain death in ICU patients: Clinical significance of endocrine changes. Indian J Endocrinol Metab 2014;18:229. 74. Singer P, Cohen J, Cynober L. Effect of nutritional state of brain dead organ donor on transplantation. Nutrition 2001;17:948–52. 75. Hergenroeder G, Ward N, Yu X, Opekun A, Moore A, Kozinetz C, et al. Randomized trial to evaluate nutritional status and absorption of enteral feeding after brain death. Prog Transplant 2013;23:374–82. 76. Novitzky D, Cooper DKC, Rosendale JD, Kauffman HM. Hormonal Therapy of the Brain Dead Organ Donor: Experimental and Clinical Studies. Transplantation [Internet]. 2006;82(11). Available from: plantjournal/ Fulltext/2006/12150/Hormonal_Therapy_of_ the_Brain_Dead_ Organ_Donor_.2.aspx. (Accessed on 03-09-2015). 77. Pinsard M, Ragot S, Mertes PM, Bleichner JP, Zitouni S, Cook F, et al. Interest of low-dose hydrocortisone therapy during brain dead organ donor resuscitation: The CORTICOME study. Crit Care 2014;18:R158. 78. Dupuis S, Amiel JA, Desgroseilliers M, Williamson DR, Thiboutot Z, Serri K, et al. Corticosteroids in the management of brain dead potential organ donors: A systematic review. Br J Anaesth 2014;113:346–59. 79. Novitzky D, Mi Z, Sun Q, Collins JF, Cooper DKC. Thyroid hormone therapy in the management of 63,593 brain dead organ donors: A retrospective analysis. Transplantation [Internet]. 2014;98(10). Available from: plantjournal/Fulltext/2014/11270/Thyroid_Hormone_ Therapy _in_the_ Management_of.17.aspx. (Accessed on 03-09-2015). 80. Orens JB, Boehler A, Perrot M de, Estenne M, Glanville AR, Keshavjee S, et al. A review of lung transplant donor acceptability criteria. J Heart Lung Transplant 2003;22:1183–1200. 81. Mascia L, Pasero D, Slutsky AS, et al. Effect of a lung protective strategy for organ donors on eligibility and availability of lungs for transplantation: A randomized controlled trial. JAMA 2010;304:2620–27. 82. Afonso RC, Hidalgo R, Paes AT, Zurstrassen MPVC, Fonseca LEP, Pandullo FL, et al. Impact of cumulative risk factors for expanded criteria donors on early survival after liver transplantation. Transplant Proc 2008;40:800–01.

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Role of Simulators in Trauma Skills and Management Training Rashmi Ramachandran, Vimi Rewari, Anjan Trikha


The traditional method of teaching with students observing the management of trauma victims and then getting involved in it directly has its flaws. The student would not have learned or practiced his skills before actually handling a real patient. This shortcoming in the traditional teaching methodology is overcome by the use of simulators.

Simulation is the act of imitating the behavior of a situation or a process by means of a suitable analogous device or system.

The simulators come in a variety of range and are classified according to their functions, use and complexity. The simulators can either be part task trainers, computer-based systems or integrated.

High fidelity simulators have especially shown significant potential as both a teaching and an assessment tool in individual and team performance in practical trauma management.

Simulators have a wide variety of utility and help not only in learning basic skills but also help in learning non-technical skills, like effective leadership, information sharing and communication with fellow team members.

INTRODUCTION Trauma has become a major global burden for morbidity and mortality. It has become the leading cause of death globally in the age group of 1–44 years.1 According to World Health Organization (WHO), road traffic accidents are the sixth leading cause of death in India. The young and middle age populace are the greatest affected by hospitalizations, disabilities and death leading to major socioeconomic loss for the country.2 Trauma-care systems in India are at a nascent stage of development. The formation and propagation of the Advanced Trauma Life Support (ATLS®) course has radically changed the perception and management of victims of trauma and injury. Similar organized measures have been successfully implemented in many other highincome countries. Development of newer teaching aids for effective training in management of trauma patients and continuous education, re-education and assessment of caregivers in management of trauma patients has been recommended for improvement in the management of patients with trauma.3

Training medical providers to care for trauma patients is a difficult task and currently used training strategies need a lot of fresh ideas and innovations to achieve optimal status. Training in trauma care has received a major boost since the onset of simulators. The traditional method of teaching with students observing the management of trauma victims and then getting involved in it directly albeit under supervision has its flaws. The student would not have learned or practiced the skills before actually handling a real patient. This shortcoming in our traditional teaching methodology is overcome by the use of simulators. Simulators are nowadays used routinely in all high stakes environment and thus are a natural choice for use in trauma management as well, and can potentially improve trauma training in a number of ways.4,5 This chapter will elucidate the various ways in which simulation and simulators can be used to improve various aspects of trauma management. SIMULATION Simulation is the act of imitating the behavior of a situation or a process by means of a suitable analogous device or

Role of Simulators in Trauma Skills and Management Training

system. The earliest used interactive simulators were probably the British wooden horse simulators used in the World War I (Fig. 35.1). The level of imitation may range from very low to very high which is the basis of classification of simulators. The wooden horse simulator, although ancient, but would probably be considered as a higher end simulator due to its interactability and its movements which were exact replica of an actual horse! Simulation has a lot of advantages over didactic teaching. The old school methodology of learning in medical education consisting of observing and then practicing on actual patients even under supervision exposes both the patient and the student to harm and stress. The simulators allow the students to learn and practice their skills before actually doing the procedure on patients. The ‘Golden hour’ in trauma patients is a critical period. Rapid assessment of life-threatening injuries, stabilization of the vital functions and deciding on the management strategies for a critically injured patient need to occur simultaneously during this short time. The management strategies are first practiced in a simulation based set-up and then the trainee is exposed to the on-site learning by observing and discussing in actual clinical setup. Simulation is also used to help them recognize the role of various members of the team managing the trauma patient by role playing models. Simulation products ranging from simple physical models to complex, computer-based virtual reality systems have been devised to aid imparting of knowledge and skills in trauma and other fields of medicine. Several of these innovations have already been shown to be as good as or better than the standard methods and have been incorporated in the standard teaching and training curriculum.


SIMULATORS The simulators come in a variety of range and are classified according to their functions, use and complexity (Table 35.1).6 Table 35.1: Classification of simulators • Indigenous simulators • Part-task trainers • Computer-based systems • Integrated simulators – Instructor driven simulators – Model driven simulators • Virtual reality and haptic systems • Simulated patients • Simulated environments

Indigenous Simulators The simplest of simulators are the ‘home made’ simulators. For example, the use of one’s own palm to simulate hard and soft palate to describe and teach insertion of laryngeal mask airways and the use of a roll of adhesive tape to simulate cricoid cartilage to teach Sellick’s maneuver. These kind of simulators can be devised using the immediately available things and can be used to demonstrate and practice basic maneuvers. Part-Task Trainers (Fig. 35.2) A higher level of simulators would be the commercially built ‘part-task trainers’. Many particular tasks and skills can be learned with the help of a model of specific portions of the patient or task. Part-task physical trainers provide only part of the model necessary for procedure or skill being learned. These trainers allow the learners to practice the diagnostic or therapeutic procedure on the model which can then be fine tuned while doing the procedures under supervision on patients. Part-task trainers of almost all the viable skills are available. A few of them useful in trauma training (Table 35.2) are mentioned below: Airway Management Trainers

Fig. 35.1: The ‘Horse’ simulator used for training soldiers during World War I

A variety of intubation, ventilation, and suction techniques can be practiced by using airway management trainers. A few of these are also available for learning insertion of supraglottic airway devices. Airway management in patients with unstable cervical injury with cervical collar, can also be taught to the learners. These trainers are available in


Essentials of Trauma Anesthesia and Intensive Care

Fig. 35.2: Part-task trainers. A, Part-task trainer for internal jugular, subclavian and basilic vein cannulation; B, Infant manikin for airway management and cardiopulmonary resuscitation; C, Part-task trainer for airway management; and D, Part-task trainer for cricothyroidotomy Table 35.2: Various part-task trainers available for trauma training Type

Part-task trainer

Utility in trauma training

Airway trainers

Airway management trainer

Practicing a variety of intubation, ventilation, suction techniques

Infant airway management trainer

Practicing basic and advanced airway management skills in infants

AirSim Advance®

Practicing nasotracheal intubation, bag and mask ventilation techniques, supraglottic device and combitube insertion apart from basic airway management skills

Cricothyrotomy simulator

Practicing cricothyrotomy with palpable landmarks including cricoid and thyroid cartilage

Central line trainer, Simulab®

Ultrasound-guided central venous access training with anatomically

Vascular access trainers


correct human torso with landmarks. Differentiates between arterial and venous blood Central line trainer, Kyoto®

Ultrasound-guided trainer allows for axillary vein approach as well as internal jugular vein approach to central venous catheterization

IV Torso®

Provides access to the external jugular vein; internal jugular vein via the anterior, central, and posterior approaches; subclavian vein; and femoral vein. A pulse bulb enables the instructor to create a palpable pulse in the manikin’s arteries

Arterial/venous Patient Arm®

Patient training arm provides pulsatile arterial blood flow for practicing venous and arterial cannulation

Echo Simulator, Vimedix®

Echocardiography training for TEE, TTE and the FAST exam on the same platform

Paracentesis Trainer®

Ultrasound compatible model allows for procedural accuracy when performing the paracentesis

Thoracocentesis Trainer®

Practicing the skills of associated ultrasound-guided thoracocentesis procedures

(The list is indicative and not exhaustive) TEE: Transesophageal echocardiography; TTE: Transthoracic echocardiography; FAST: Focused assessment sonography in trauma.

Role of Simulators in Trauma Skills and Management Training

both pediatric and adult models. Procedures, like cricothyroidotomy, percutaneous tracheostomy and conventional emergency tracheostomy, can also be done on either the same or different dedicated models. Vascular Access Trainers These trainers are models of an arm, mid-torso or the neck and chest segment of human body. They are useful for both arterial and venous cannulation. The models may be dedicated for either peripheral or central venous catheter (CVC) cannulation. Cannulation of external and internal jugular, axillary, subclavian and femoral veins can be taught and practiced on these trainers. In some newer models, it is possible to visualize the vessels by ultrasound and learning and training of ultrasound-guided cannulation is also possible. Thoracocentesis and Thoracostomy Trainers These models allow users to develop and practice the skills necessary to gain expertise in identifying and guiding needle and catheter insertions in the patient with pleural effusion. Many models are available which allow both ultrasoundguided and non-ultrasound guided thoracocentesis and thoracostomy to be done by learners. Pericardiocentesis and Paracentesis These models allow the performance of removal of fluid filled in pericardium and abdomen, respectively. As with thoracocentesis trainers, they are also available in versions which may allow the learners to perform the procedures under ultrasound guidance. The abdominal trainers which allow visualization of ultrasound images can also be used for training in focused assessment sonography in trauma (FAST). Computer Based Systems Computer systems can be used to replicate various characteristics of human physiology and pharmacology as well as the surrounding environment. These are then used for interaction with the learner through a computer screen. These types of simulators can be run in a desktop computer using only a screen, a pointing device. Patient voice is provided with the help of integrated audio inputs and outputs and patient profile can be seen via animation, drawings or video. The learner can communicate with the ‘patient’ by asking questions (typing or speaking). Various patient-related data, like laboratory reports, X-rays and results of various diagnostic tests, are also made available on the monitor.


Therapeutic actions can be performed on the ‘patient’ by making choices with the mouse. There are no manikins in this kind of simulators. The only purpose of the teaching exercise is helping the student learn the usage of information to make treatment decisions and observe their implicit effect through computer interface. Students are provided with feedback of their decisions and performance during or after the interaction. Computer-based systems are relatively inexpensive, easy to use, can be used by multiple learners and requires less hardware handling and less personnel to man the simulator sessions. These systems are more useful than didactic lecture sessions in learning management of various problem-based events. For example, the computer interface describes the injury event and the related cardiovascular physiology of a patient who has undergone trauma. The learner is now required to give input of various management steps. Each step is analyzed by the computer and results in change in physiology of the patient. The learner thus can observe the results of the intervention proposed by him/her simultaneously as the event progresses. An example of such a system can be seen at: resus/moulage/moulage.html. Integrated Simulators Integrated simulators combine both a computer and manikin or part of it on which to carry out interventions. Interventions are carried out on the manikin which produces physical signs and feed physiological signals to the integrated patient monitors with the help of computer. The degree of fidelity or imitation depends on the level of complexity of the manikin and the computer that drives the whole system. Many terms are used to describe this level of simulator; however, they are most easily classified by their ‘driver’ or the medium of control. Instructor driven or the ‘intermediate fidelity’ simulators combine part or full body manikins with computer interface and programs. The computer software produces physiological signals that are displayed on a computer screen which is an analog for patient monitor. The clinical parameters of the patient or the manikin are, however, adjusted by an instructor who also adjusts these parameters according to the event or scenario being projected for the learners (unlike the model driven simulators where the clinical parameters reflect the models own physiology). These simulators are less complex in terms of hardware and software components and thus are of relatively less cost as compared to the high-fidelity simulators.


Essentials of Trauma Anesthesia and Intensive Care

Model driven or the ‘high fidelity’ patient simulators combine sophisticated life-like manikins with complex computer programs driving the manikin’s respiratory and cardiovascular physiology (Fig. 35.3). These manikin-based simulators can replicate many intricate patient aspects, like spontaneous respiration (and the ability to ventilate the patient with a rebreathing bag or ventilator), real-time display of electronically monitored information [e.g. electrocardiography (ECG), oxygen saturation, etc.] peripheral and central pulses, heart sounds, breath sounds, pupil size, pupillary response to light and airway obstruction at various levels. They have intricate programming to produce dynamic effects of various drugs on the cardiovascular, respiratory and neuromuscular physiology of the manikin. The clinicians or the learners interact with the ‘manikin’ as they would do so with a patient in the real clinical setup. Loudspeakers placed in the manikin’s head portion create the impression of the ‘patient’ talking. Clinical parameters including palpable pulse, breathing excursions, heart sounds, pupillary reactions and urine output are simulated in this sophisticated manikin. The clinical monitors receive the physiological signals generated by the manikin (analogous to those used in actual operation theaters and other clinical areas), allowing monitoring, like ECG, non-invasive blood pressure, oxygen saturation, central venous pressure, pulmonary artery and intracranial pressure, to be carried out. The manikin will automatically ‘sense’ the drugs injected into the drug port and have appropriate effects through the interaction between the computer programming and manikin features. The clinician undergoing the simulation practice

Fig. 35.3: High fidelity human patient simulator. Note the real anesthesia machines and ventilator with the monitor showing actual ‘patient’ parameters. The manikin and the accessories are placed in a real operation theater setup

session is expected to intervene on the manikin according to the changing information from the patient and monitors. These interventions may include, but are not limited to, oxygen supplementation, endotracheal intubation or chest tube drain insertion. The complex computer system modeling allows the manikin to have the appropriate physiological or pharmacodynamic effects automatically. For example, increasing the fraction of inspired oxygen concentration will increase the oxygen saturation of the manikin which is displayed on the patient monitor, fluid administration will correct hypovolemia and the administration of adrenaline will cause increases in blood pressure and heart rate, so on and so forth. Early data on the use of high fidelity simulators for trauma training suggest an advantage over traditional moulage setting teaching practices.7 Model-driven simulators are, however, very costly because of the complex programming, hardware and software requirements. They also need a team of simulation experts, technicians and ancillary support staff for their management and upkeep, making them useful only in institutional setups. The METI Human Patient Simulator (HPS®), Emergency Care Simulator (ECS®), PaediaSim® and the MedSim Patient® are examples of commercially available high fidelity simulators. Integrated Simulators Especially Developed for Trauma Training 1. The Trauma Man®: System made by Simulab, USA, is an anatomical surgical manikin that is designed for students to practice various surgical procedures. This system has been evaluated and approved by the American College of Surgeons in 2001 as a substitute to live nonhuman models or cadavers for the ATLS® course. Since its release, TraumaMan is also being used widely in military courses, emergency medical services (EMS) training, and other trauma surgery simulation training programs. The system consists of a replicated human torso with a ventilator and four anatomically correct surgical zones and an ankle base for intravenous cutdown. Procedures, like cricothyroidotomy, thoracocentesis, pericardiocentesis, needle decompression, percutaneous tracheostomy, diagnostic peritoneal lavage, intravenous cutdown and wound suturing, can be practiced on it. It also has a FAST diagnostic ultrasound training extension which allows learners to identify landmarks on the body used for identification of window locations for the examination and read and understand the various normal and abnormal views seen during the ultrasound examination.

Role of Simulators in Trauma Skills and Management Training

2. SimMan 3G Trauma®: A Laerdal product, SimMan 3G is meant for specialist use as a trauma patient simulator specifically designed for military and civilian emergency services. It is light weight and portable and is well suited for training the rapid assessment of trauma emergencies. It also simulates necessary interventions, such as hemorrhage control and airway management. SimMan 3G Trauma has some essential features, such as amputated limbs and sternal intraosseous access to provide training for management of bleeding trauma emergency situations. This simulator is routinely used in hospitals, ambulances and in military combat environment for imparting training and practicing management of trauma patients. 3. HydraSim Trauma Bleeding Simulation System® from Skedco, Inc., Oregon, USA is a simulation aid rather than an integrated simulator. It looks like a common backpack hydration system and can provide 3 liters of blood pumping at high intensity. The HydraSim®is attached to low fidelity training manikins making them higher fidelity. Its blood pumping special effect from multiple bleeding wounds gives the users have the opportunity to practice treatments ranging from junctional or non-junctional tourniquet application to wound packing and application of dressing. This simulation aid is useful in training students the management of massive hemorrhage and transfusion protocols. 4. Caesar® by CAE Saint-Laurent, Quebec, Canada, is built for trauma, disaster response and combat casualty care. It is a rugged patient simulator with life-sized realism and modeled physiology. Like SimMan 3G Trauma, this can also be deployed in any challenging climate, terrain or training environment for basic to advanced on-site training. 5. TraumaF/X® has been jointly developed by the US Army ARL-STTC and consists of a line of manikins used in both military and civilian training. 6. Trauma HAL® made by Gaumard Scientific, USA, is a tetherless trauma simulator. This again is a rugged simulator and can be used in field situations. It can be moved easily from the accident scene to the emergency room (ER), to the intensive care unit (ICU), while care providers diagnose and treat the simulated patient’s condition using real monitoring and resuscitation equipment.


Virtual Reality and Haptic Systems Virtual reality refers to a set of techniques in which one interacts with a synthetic or ‘virtual’ environment that exists solely in the computer. In the typical conception of virtual reality, the representation of the environment is fed directly to the eyes, ears and possibly hands of the perpetrator. Virtual reality is an advanced computer-based technology. Its main aim is to present virtual objects or environments to all human senses in a way which is similar to their natural counterpart. Such computer generated models are often used in combination with part-task trainers to allow a physical interaction to take place within the virtual environment. This technology is used extensively in the expanding field of laparoscopic and endoscopic dexterity trainers. Their use in military training for simulating difficult and dangerous situations is also well utilized and established. The widespread use of these simulators are, however, limited by their exorbitant cost included in both establishment and running of such simulators. They would indeed be extremely useful in trauma training especially the on-site or pre-hospital management.8 UTILITY OF SIMULATORS IN TRAUMA TRAINING Basic Skills Teaching The part-task trainers are particularly useful in learning the basic clinical skills essential for initial management of patients with trauma. The part task trainers are used for teaching airway management (use of oral airways, supraglottic airways and endotracheal intubation). They are particularly useful in procedures, like cricothyroidotomy and percutaneous tracheostomy, which are time sensitive and extremely useful emergency airway management techniques. Airway management along with procedures, like application of manual in-line stabilization and semi-rigid cervical collars in patients with suspected cervical spine injury, can also be taught with the help of airway trainers. Part-task trainers can also be used for imparting training in various basic and useful skills including peripheral and central venous accesses, thoracocentesis, thoracostomies and pericardiocentesis. A recent systematic review and metaanalysis analyzed the intervention of simulation on participants undergoing training for invasive vascular procedures. The comparator in all the studies that were included was nonsimulation training. Proportion of overall success in completion of CVC insertion on real patients was higher in the simulation group than the traditional group (89.8% vs.


Essentials of Trauma Anesthesia and Intensive Care

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